THE  LIBRARY 

OF 

THE  UNIVERSITY 

OF  CALIFORNIA 

LOS  ANGELES 

GIFT  OF 

SAN  FRANCISCO 
COUNTY  MEDICAL  SOCIETY 


, 


LOCOMOTOR  ATAXIA 

(Tabes  Dorsalis) 


AN  INTRODUCTION  TO  THE  STUDY  AND 
TREATMENT  OF  NERVOUS  DISEASES, 
FOR  STUDENTS  AND  PRACTITIONERS 


BY 
WILLIAM  J.  M.  A.  MALONEY,  M.D.  (EDIN.) 

FELLOW  OF  THE  ROYAL  SOCIETY  OF  EDINBURGH ;   FELLOW  OF  THE  NEW 
YORK  ACADEMY  OF  MEDICINE;  FELLOW  OF  THE  NEW  YORK  NEURO- 
LOGICAL SOCIETY:  NEUROLOGIST  TO  THE  CENTRAL  AND 

NEUROLOGICAL  HOSPITAL;    FORMERLY  PROFESSOR 

OF    NEUROLOGY,    FORDHAM    UNIVERSITY, 

NEW   YORK   CITY 


ILLUSTRATED 


D.  APPLETON  AND  COMPANY 

NEW  YORK  LONDON 

1918 


COPYRIGHT,  1918,  BY 
D.  APPLETON  AND  COMPANY 


Printed  in  the  United  States  of  America 


TO 

VICTOR  EDGAR  SORAPURE,  M.B., 
F.R.C.S.  (EDIN.), 

SOMETIME 
PROFESSOR  OF  CLINICAL  MEDICINE 

AND 

PRO-DEAN  OF  THE  FACULTY  OF  MEDICINE, 

FORDHAM  UNIVERSITY, 

NEW  YORK  CITY 


We 


PREFACE 

As  the  brilliant  researches  of  Sherrington  upon  reflex  func- 
tion, of  Head,  Holmes,  Sherren  and  their  co-workers  upon  sen- 
sory function,  and  of  Langley,  Gaskell,  Biedl,  and  Gley  upon 
vegetative  function,  have  revolutionized  our  knowledge  of  ner- 
vous phenomena,  it  is  now  essential  to  restudy  every  nervous 
disease,  to  interpret  its  symptoms  with  the  aid  of  this  new  knowl- 
edge, and  to  organize  its  treatment  according  to  the  new  inter- 
pretation. 

This  book  correlates  our  present  anatomical,  pathological, 
physiological,  and  psychological  knowledge  with  reference  to 
locomotor  ataxia.  The  correlation  has  been  planned  solely  with 
a  view  to  treatment.  Matters  having  no  direct  bearing  on  treat- 
ment do  not,  therefore,  receive  the  attention  which  they  usually 
enjoy  in  text  books  on  nervous  diseases. 

As  a  student  I  suffered,  in  common  with  every  other  student, 
from  inability  to  understand,  through  my  training  in  anatomy 
and  physiology,  the  clinical  evidence  of  nervous  diseases.  So 
nervous  diseases  then  interested  me  mainly  as  a  compulsory  exer- 
cise in  memory,  decreed  by  captious  examiners.  The  student's 
lack  of  power  to  apply  knowledge  is  recognized  by  all  teachers. 
It  is  inherent  to  the  phase  of  being  taught.  A  mind  attuned  to 
acquire  facts  in  bulk  cannot  simultaneously  fix  and  correlate 
them. 

After  his  preliminary  training  in  the  fundamental  sciences 
of  anatomy,  physiology,  pathology  and  psychology,  the  student 
should  be  taught,  from  a  concrete  example,  how  normal  structure 
varies  in  nervous  disease;  how,  from  this  anatomical  variation, 
physiological  and  psychological  consequences  follow  which  make 
the  symptoms  inevitable  and  the  treatment  effective.  With  this 
training  he  will  intelligently  approach  any  nervous  diseases  he 
may  subsequently  encounter;  he  will  become  a  thinking  instead 
of  an  automatic  physician,  and  nervous  diseases  will  so  interest 
him  that  much  of  their  difficulty  will  disappear. 

The  student's  royal  road  to  the  understanding  of  nervous 
diseases  lies  through  tabes.  In  tabes  there  are  demonstrable  the 


603496 


viii  PREFACE 

exciting  cause — the  spirochete,  the  lesions — the  structural  effect 
of  that  cause,  and  the  physiological  and  psychological  conse- 
quences of  these  lesions.  Reflex  integration  and  its  disturbance, 
interruption  of  sensory  and  of  motor  paths,  vegetative  disorders, 
and  the  interaction  of  the  psyche  with  the  sensory,  motor,  and 
vegetative  nervous  systems,  all  can  be  presented  connectedly  and 
concretely  to  students  through  the  study  of  tabes. 

Indeed,  there  are  few  facts  in  neurology  which  cannot  be 
demonstrated  in  tabes;  and  there  are  few  nervous  diseases  so 
amenable  to  treatment  as  it  is.  The  physiological  and  psycho- 
logical basis  of  the  treatment  is  obvious ;  the  results  seem  often 
miraculous.  Students  trained  in  neurology  through  the  teaching 
of  tabes  respect  the  science,  value  it,  and  practice  it. 

Hence  I  explain  the  physiology  and  the  psychology  of  func- 
tion in  detail  which  would  be  unnecessary,  were  I  writing  solely 
for  my  present  and  not  also  for  my  future  colleagues.  I  espe- 
cially emphasize  the  role  of  the  vegetative  nervous  system,  partly 
because  of  our  former  neglect  of  it,  but  mainly  because  of  the 
superlative  importance  it  has  not  only  in  producing  the  symp- 
toms but  likewise  in  permitting  the  disease. 

There  is  a  psychological  as  well  as  a  physiological  element  in 
all  symptoms,  in  all  disabilities.  Psychological  treatment  is, 
therefore,  as  essential  as  physiological  treatment.  In  many  medi- 
cal cases  psychological  treatment  is  the  only  treatment  neces- 
sary, and  in  some  of  the  others  it  is  the  only  treatment  possible. 
By  those  who  ordain  the  medical  curriculum,  physicians  are, 
presumed  to  be  endowed  with  the  art  of  psychological  treat- 
ment. We  might  as  well  be  presumed  to  inherit  the  healing 
touch.  Psychotherapy  must  be  taught  in  the  schools  or  medi- 
cine cease  to  be  a  legally  restricted  profession. 

Upon  the  reciprocal  relations  of  the  mental  state  and  the 
tabetic  symptoms,  and  upon  the  interdependence  of  the  symp- 
toms, rests  the  basis  of  psychological  treatment.  "Without  knowl- 
edge of  these  relations,  effective  treatment  is  impossible. 

Treatment  based  on  these  relations  does  not  lead  to  radical 
cure,  to  the  removal  of  lesions.  But  we  can  rarely  remove 
nervous  lesions;  and  often  it  is  mainly  the  mental  reaction  to 
lesions  which  determines  the  pain  or  ease,  the  misery  or  com- 
fort of  patients.  Psychic  treatment  counteracts  unfavorable 
mental  reactions  and  thus  minimizes  the  influence  of  lesions. 
It  further  educates  the  patient  to  control  residual  symptoms, 


PREFACE  ix 

to  protect  himself  against  their  aggravation;  and  when  such 
aggravation  does  occur  it  enables  him  quickly  to  alleviate  it. 

I  systematize  the  application  of  this  knowledge,  for  the  prin- 
ciples upon  which  the  tabetic's  treatment  is  founded  are  not 
restricted  in  their  usefulness  to  tabes.  They  are  obviously  appli- 
cable to  the  treatment  of  all  conditions  in  which  the  mental  state 
aggravates  symptoms,  or  in  which  symptoms  threaten  the  in- 
tegrity of  the  mental  state. 

The  method  of  treating  ataxia  wrhich  I  have  advocated  since 
1912,  and  which  I  now  fully  describe  for  the  first  time,  is  based 
on  the  thesis  that  perfect  thinking  is  essential  to  perfect  moving ; 
and  perfect  moving  is  the  outward  sign  of  perfect  thinking. 
Training  in  perfect  thinking  is,  therefore,  training  in  perfect 
moving ;  and  training  in  perfect  moving  is  training'  in  perfect 
thinking.  The  details  of  the  training  and  the  measures  needed 
to  ensure  optimal  conditions  for  it,  I  have  carefully  outlined. 

In  this  material  and  impious  age  the  Jordan  flows  unheeded 
and  the  waters  of  Bethesda  rise  unwatched.  Healing  words  re- 
place healing  waters.  Religion  and  health  are  unhappily  con- 
founded by  those  who  foster  the  Emanuel  movement  and  by  the 
earnest  members  of  that  faith  which  is  disguised  as  science  and 
called  Christian.  Where  remorse  is  morbid,  or  suffering  is  due 
to  ignorance  of  Divine  love,  ecclesiastical  ministration  is  proper 
and  pertinent ;  beyond  these  limitations,  it  is  ultimately  destruc- 
tive to  the  faith  which  excuses  it  and  to  the  health  which  it 
seeks.  Medical  inadequacy  led  to  these -movements;  the  measure 
of  their  success  is  the  measure  of  our  failure. 

The  cause  of  our  failure  is  neglect  of  the  study  of  the  recipro- 
cal relations  of  symptoms  and  mental  states.  The  unauthorized, 
ignorant  of  the  source  of  symptoms,  but  efficient  in  molding  the 
mental  state  of  the  faithful,  bring  relief  to  those  whom  mis- 
guided medical  effort  has  failed  to  ease.  It  is  a  matter  of  con- 
gratulation for  all  when  suffering  is  relieved  by  any  one.  A 
sufferer  has  an  inalienable  right  to  seek  relief  at  any  source. 
We  cannot  continue  to  preempt  the  power  to  heal  when  others 
succeed  where  we  fail,  nor  can  the  community  allow  suffering  to 
be  subject  to  the  ignorant. 

To  his  science  no  less  than  to  ,his  conscience  the  physician 
owes  the  duty  of  giving  mental  ease  to  his  patient.  That  ease 
must  be  given,  not  through  stupefying  with  mystic  incantations 
and  irrational  suggestions,  but  by  rousing  the  patient  to  the  na- 


x  PKEFACE 

ture  of  his  danger  and  by  teaching  him  to  organize  his  own 
defense. 

Only  through  mental  training  will  the  sick  unfailingly  receive 
aid  in  defending  themselves  against  the  tyranny  of  symptoms. 
Defense  based  upon  self-control  over  mental  processes  is  more 
potent  and  permanent  than  that  afforded  by  the  degrading  and 
treacherous  support  of  suggestion,  and  more  worthy  and  secure 
than  that  which  is  founded  upon  ignorant  mysticism. 

The  source  of  each  borrowed  illustration  is  indicated  in  its 
caption.  I  am  grateful  to  the  several  authors  whose  illustrations 
I  have  used. 

I  am  indebted  to  Doctor  Abrahamson,  Professor  of  Clinical 
Neurology  at  Bellevue  Medical  School,  Neurologist  to  the  Central 
and  Neurological,  Montefiore,  and  Mount  Sinai  Hospitals,  New 
York  City.  His  great  experience  and  knowledge  were  always 
at  my  service  and  were  of  invaluable  assistance  in  many  difficul- 
ties. Doctors  Grossman  and  Wolf  have  earnestly  worked  with 
me  and  the  former  has  kindly  placed  some  excellent  photographs 
at  my  disposal. 

Years  ago,  when  I  was  the  Crichton  Research  Fellow,  Doctor 
C.  C.  Easterbrook,  the  distinguished  director  of  the  Crichton 
Royal  Institution,  Dumfries,  Scotland,  stimulated  me  with  his 
great  enthusiasm  for  applied  psychology.  The  length  of  my 
latent  period  is  due  mainly  to  the  war;  to  that  cause  also,  I 
hope,  he,  kindliest  of  critics,  will  attribute  what  is  lacking  in  the 
following  pages. 

.  Doctor  H.  R.  Storer  of  Newport,  Rhode  Island,  kindly  cor- 
rected the  proofs. 

WILLIAM  J.  M.  A.  MALONEY 
156  East  79th  Street 

New  York  City 


CONTENTS 


I.— THE  SPIROCHETE  AND  TABES.  THE  SITE  OF  THE 
STRUCTURAL  CHANGES  PRODUCED  BY  THE 
SPIROCHETE  IN  THE  CENTRAL  NERVOUS 
SYSTEM 1 

Discovery  of  tabes.  Controversy  concerning  its  cause.  Rela- 
tion of  tabes  to  syphilis.  The  Spirochaeta  pallida,  the  ex- 
citing organism  of  tabes.  Strains  of  spirochete.  Spirochetes 
that  persist  in  the  human  host  and  attack  tissues  usually 
immune.  The  three  varieties  of  the  persisting  spirochete. 
The  attacking  force  of  the  persisting  spirochete.  Invasion 
by  the  persisting  spirochete  of  vascular,  glandular  and  ner- 
vous tissues.  Causes  which  determine  that  the  major  attack 
shall  fall  upon  the  central  nervous  system.  The  spirochete's 
invasion  not  restricted  to  any  one  area  in  the  central  nervous 
system.  Factors  which  determine  the  initial  site,  the  extent 
and  the  direction  of  the  spirochete  invasion  in  the  central 
nervous  system. 

IL— RESULTS  OF  THE  SYPHILITIC  LESIONS:  DIS- 
TURBANCE OF  THE  REFLEX  MOTOR  FUNCTION  18 

The  posterior  root  ganglion  and  coverings.  Ganglion  cell 
lesions.  Meningeal  lesions.  The  posterior  root  itself  a  pri- 
mary site  of  spirochete  invasion.  Nature  and  result  of  the 
syphilitic  change  in  the  posterior  root.  The  sensory  nerve 
of  muscle.  The  simple  reflex  arc  of  muscle  tone.  The  func- 
tional linking  of  reflex  arcs.  The  knee-jerk,  its  relation  to 
the  reflex  arc  of  muscle  tone,  its  governing  factors.  Altera- 
tions of  tendon  reflexes  in  tabes.  Hypotonia :  effect  on 
strength  and  mobility  of  joints.  Dislocations.  Contortions. 
Muscular  weakness  of  tabes;  causes.  Disintegration  of 
reflex  function.  Influence  of  extent,  rapidity,  site  and  dura- 
tion of  the  lesions.  Measurement  of  the  amount  of  the  dis- 
turbance. Identical  motor  effects  produced  by  reflex  and  by 
cortical  action.  Site,  paths  and  nature  of  cerebral  control 
of  movement.  Reflex  defects  masked  during  voluntary  move- 
ment. 

xi 


xii  CONTENTS 

CHAPTER  PAGE 

III.— RESULTS    OP    THE    SYPHILITIC    LESIONS:     DIS- 
TURBANCE OF  SENSORY  FUNCTION     ...      45 

Course  of  the  sensory  impulses  from  the  periphery  to  con- 
sciousness. Specific  nature  of  the  impulses  conducted  by 
sensory  fibers.  Sensory  images.  Factors  which  determine 
the  fate  of  the  sensory  images.  The  peripheral  impulse  and 
the  mental  reaction  to  it.  Measurement  of  stimuli.  Sensory 
thresholds;  their  variability.  Complex  content  of  the  sensa- 
tion which  arises  from  a  simple  stimulus.  Sensory  results 
of  a  complete  and  of  an  incomplete  lesion  of  the  posterior 
root.  Selective  invasion  of  the  root  fibers  conducting  pain. 
Touch  loss.  Temperature  loss.  Vibration  loss.  The  postural 
sense.  Paths  of  sensory  fibers  from  the  muscular  apparatus 
and  from  the  postural  sense  organ  of  the  head.  Loss  of  the 
sense  of  the  body's  posture.  Measurement  of  the  loss  of  pos- 
tural sense.  Effect  of  blindness  and  of  training  on  postural 
sense  in  the  non-tabetic  and  in  the  tabetic.  Variability  of 
postural  sense  loss.  Postural  sense  loss  inaccurate  index  of 
the  severity  of  the  tabetic  lesions. 

IV.— RESULTS    OF    THE    SYPHILITIC    LESIONS:     DIS- 
TURBANCES OF  ATTITUDE  AND  MOVEMENT      .      61 

The  changing  and  maintaining  of  attitude.  Attitude  ex- 
pressive of  the  motor  tendencies  that  we  desire  and  of  those 
that  are  unconsciously  evoked  by  the  mental  state.  The 
impossibility  of  maintaining  an  immovable  posture.  Normal 
swaying.  Tabetic  swaying,  Romberg's  sign.  The  tabetic  atti- 
tude. Effect  of  blindness,  psychotherapy  and  mental  states 
on  the  tabetic  attitude.  The  tabetic  attitude  a  consequence 
not  only  of  the  lesions  but  also  of  the  mental  state.  Ataxic 
movements.  Controversy  regarding  the  cause  of  ataxia. 
Importance  of  the  constituent  parts  of  the  muscular  appa- 
ratus in  coordination.  Postural  sense  loss  not  parallel  to 
ataxia.  Reflex  defect  not  necessarily  associated  with  ataxia. 
Onset  and  course  of  ataxia.  Fatigue,  fear  and  shock  as  pre- 
cipitants  of  ataxia.  The  ataxic  moment.  The  relation  of 
ataxia  to  the  tabetic  lesions.  Psychic  control  of  coordination. 
The  ratio  between  effort  and  accomplishment  in  movement. 
Voluntary  movement  the  resultant  of  the  desired  and  of  the 
unconsciously  evoked  postural  images.  The  interaction  of 
voluntary  and  of  reflex  movement.  Psychic  activity  mask- 
ing reflex  defect  in  voluntary  movement  throughout  the  pre- 
ataxic  stage.  Ataxic  complexes.  Coefficient  of  ataxia.  The 


CONTENTS  xiii 

CHAPTER  PAGE 

reciprocal  relations  of  ataxia  and  the  mental  state.  The 
amount  of  disturbance  of  attitude  and  movement  mainly  a 
measure  not  of  the  structural  changes  but  of  the  degree  of 
the  failure  of  conscious  control  of  movement  to  compensate 
for  the  tabetic  defect  in  the  reflex  mechanism.  The  sur- 
render or  so-called  paralytic  stage. 

V.— RESULTS     OF     THE     SYPHILITIC     INVASION   OF 

CRANIAL  NERVES 86 

The  olfactory  nerve.  The  optic  nerve.  Onset,  course  and 
nature  of  optic  atrophy.  Ophthalmoscopic  findings.  Psychic 
and  structural  factors  in  visual  loss.  Effect  of  mescalin  in 
enhancing  vision.  Difficulty  of  measuring  visual  acuity. 
Measurement  of  light  perception  in  nearly  blind  tabetics. 
Threshold  of  perception  of  light,  threshold  of  perception  of 
change.  Blindness :  frequency,  time  of  onset,  rate  of  develop- 
ment. Causes  of  spontaneous  improvement  in  visual  acuity. 
Absence  of  proof  that  optic  tabes  arrests  spinal  tabes.  In- 
fluence of  blindness  upon  ataxia.  Spontaneous  cure  of 
ataxia  following  blindness.  Influence  of  blindness  upon  the 
mental  state  and  upon  sensory  perception.  The  relation  of 
loss  of  vision  to  coordination.  Effect  of  blindness  upon 
pain  and  deafness.  Third,  fourth,  and  sixth  nerves. 
Diplopia,  its  causes,  squint,  spontaneous  cure.  Means  for 
ascertaining  the  presence  of  suppressed  visual  images.  The 
fifth  nerve.  The  seventh  nerve.  The  eighth  nerve.  Vestib- 
ular  lesions.  Auditory  mechanism.  Psychic  deafness. 
Tabetic  deafness.  Influence  of  deafness  upon  the  mental 
state.  Increase  of  deafness  with  stationary  lesions.  Other 
cranial  nerves. 

VI.— RESULTS  OF  THE  SYPHILITIC  LESIONS  OF  THE 
VEGETATIVE  NERVOUS  SYSTEM:  SENSORY 
AND  MOTOR  DISTURBANCES  .  .  .  .116 

The  correlation  of  cells.  Development  of  the  primitive  vege- 
tative nervous  system.  The  vegetative  nervous  system  in  man 
composed  of  two  antagonistic  components,  the  vagal  and  the 
sympathetic.  Action  of  these  components  illustrated  by  the 
pupil.  The  pupil  in  tabes.  Vegetative  reflex  arcs  and  plex- 
uses. The  afferent  and  efferent  fibers  linking  these  arcs  with 
so-called  "centers"  in  the  central  nervous  system.  Tracing 
of  the  sensory  fiber.  Proof  that  pain  from  pressure  on  the 
face  passes  not  by  the  fifth  but  by  the  sympathetic.  Pres- 


xiv  CONTENTS 

CHAPTER  PAGE 

sure  pain  loss  in  tabes  on  limbs,  eyes,  testicles  and  other 
viscera.  Loss  of  visceral  reflexes.  Lightning  pains,  charac- 
ters and  frequency:  their  source  in  irritation  of  the  vege- 
tative nervous  system.  Lightning  pains  and  crises  allied 
phenomena.  Gastric,  rectal,  bladder  and  genital  crises. 
Pains  and  crises  reciprocally  related  to  the  mental  state. 
The  physiology  of  micturition.  Micturition  in  tabes. 

VIL— RESULTS  OF  THE  SYPHILITIC  LESIONS  OF 
THE  VEGETATIVE  NERVOUS  SYSTEM:  DIS- 
TURBANCES OF  CHEMICAL  CORRELATION  .  135 

Action  of  the  products  of  the  internal  secreting  glands.  The 
antagonistic  reaction  to  chemical  substances  shown  by  the 
vagal  and  the  sympathetic  components  of  the  vegetative 
nervous  system.  Oscillations  in  the  balance  between  vagal 
and  sympathetic  components,  due  to  chemical  stimuli,  con- 
trol metabolism,  and  defense  against  organismal  invasion. 
Disturbance  of  this  control.  Trophic  conditions:  ulcers,  in- 
fections, fractures,  arthropathies.  Defense  against  the 
spirochete.  Production  of  defense  substances.  Stimulation 
of  vegetative  nervous  system  by  defense  substances.  Ade- 
quate stimulation  causing  perfect  defense.  Inadequate  stimu- 
lation permitting  persistence  of  the  spirochete.  Inadequate 
stimulation  due  to  mildness  of  pretabetic  lesions,  to  glandular 
insufficiency,  to  age,  to  mental  stress.  Imperfect  defense, 
causes.  Effect  of  lesions  of  vegetative  nervous  system  upon 
defense.  Why  optic  tabes  is  abortive.  Why  the  vegetative 
nervous  system,  although  the  first,  is  not,  as  a  rule,  the 
main  site  of  spirochete  invasion. 

VIII.— DIAGNOSIS  AND  COURSE  OF  TABES    .   .   .151 

Symptoms  and  signs  of  tabes;  their  origin.  Diagnosis  of 
syphilis.  First  sign  of  invasion  of  nervous  system.  Course 
of  invasion  beginning  in  posterior  root;  beginning  in  optic 
nerve.  Tabes  diagnosed  by  evolution.  Tabes  a  disease  in 
which  dominant  symptoms  arise  from  primary  syphilitic 
invasion  of  posterior  nerve  roots.  Pretabetic  period,  dura- 
tion and  significance.  Effect  of  age  on  pretabetic  period. 
Rate  of  syphilitic  invasion.  Rapid,  slow  and  abortive  inva- 
sions. Remissions.  Preataxic  stage.  Ataxic  stage.  "Para- 
lytic" or  surrender  stage.  These  stages  psychological,  not 
anatomical.  Types  of  tabes.  Age  of  onset  of  tabes.  Ter- 
mination of  tabes. 


CONTENTS  xv 

CHAPTER  PAGE 

IX.— ANTISYPHILITIC  TREATMENT  IN  TABES        .        .    165 

Essential  tabetic  lesion  irreparable.  Tabes  incurable.  Effect 
of  antisyphilitic  treatment  on  the  duration  of  the  pretabetic 
period.  Absence  of  proof  that  such  treatment  can  prevent 
tabes.  Nature  of  the  evidence  required  to  establish  such 
preventive  action.  Absence  of  proof  that  antisyphilitic 
substances  arrest  tabes.  Nature  of  the  evidence  required  to 
establish  the  power  of  a  drug-  to  arrest  tabes.  Drugs  com- 
monly used  in  tabes.  Mercury:  modes  of  administration. 
Arsenic,  enesol,  salvarsan.  Motives  for  intraspinal  admin- 
istration unfounded.  The  search  for  new  preparations  of 
antisyphilitic  substances  and  for  new  methods  of  adminis- 
tration: indications  of  the  inadequacy  of  these  substances. 
Necessity  for  caution  in  the  use  of  mercury  and  arsenic 
in  tabes.  Nucleinates  and  nucleinic  acid. 

X.— THE  MENTAL  STATE  OF  TABES 176 

Mental  stress  a  cause  of  tabes.  Tabes  a  source  of  mental 
stress.  Tabes  a  cause  of  fear,  of  fatigue,  and  of  depression. 
Psychoses  in  tabes.  The  psychosis  typical  of  tabes  an  aggra- 
vation of  the  mental  state  induced  by  the  tabetic  symptoms. 
Resemblance  between  tabetic  psychoses  and  prison  psychoses. 
Measurement  of  the  mental  state  of  the  tabetic.  Weakening 
of  attention  in  tabes :  its  sensory  and  motor  effects.  Varia- 
tions in  the  mental  state  of  tabes.  Mental  deterioration : 
its  rate  and  its  consequences.  Influence  of  the  tabetic  symp- 
toms upon  the  mental  state.  Influence  of  the  mental  state 
upon  the  tabetic  symptoms.  Estimation  of  the  reciprocal 
relations  of  the  tabetic  symptoms  and  the  mental  state. 
Interdependence  of  tabetic  symptoms.  Foundations  of  men- 
tal treatment. 

XI.— TREATMENT  OF  THE  MENTAL  STATE:  TREAT- 
MENT OF  THE  SYPHILITIC  NEURASTHENIC 
AND  OF  THE  PREATAXIC  TABETIC  0  .  190 

Imperative  necessity  for  treatment  of  syphilitic  neuras- 
thenia, the  precursor  of  tabes  and  paresis.  Principles  of 
treatment:  rest,  reduction  of  effort  to  capacity,  avoidance 
of  harmful  thinking,  training  in  mental  control,  freedom 
from  unnecessary  medical  interference.  .  Treatment  of  the 
preataxic  tabetic.  Prosecution  for  syphilis.  Communicating 
the  diagnosis.  Reducing  mental  expenditure.  Isolation  and 


xvi  CONTENTS 

CHAPTER  PAGE 

imprisonment.  Immobilization  and  rest.  Effect  of  attitude 
in  perpetuating  and  aggravating  stress.  The  teaching  of 
rest.  Rest  exercises,  respiratory  and  muscular.  Psychological 
and  physiological  effect  of  the  exercises,  effect  on  blood 
pressure,  pulse  rate  and  pulse  rhythm.  Exercises  in  eon- 
trolling  mental  processes  through  movement.  Respiratory 
exercises,  pneumograph.  Head  exercises,  cephalograph.  Eye 
exercises.  Exercises  in  mental  work.  The  reckoning  test.  The 
daily  schedule.  Results  and  duration  of  regime.  The  transi- 
tion period.  The  return  to  business  and  social  life.  System- 
atizing and  limiting  daily  effort.  Importance  of  practicing 
the  exercises  to  prevent  relapses  and  to  avoid  ataxia. 

XII.— PSYCHOTHERAPY  OF  PREATAXIC  SYMPTOMS      .    214 

Preataxic  symptoms.  Diplopia.  Pain,  measurement  and 
analysis.  Treatment  of  subacute  pain ;  of  pain  crises.  Gastric 
crises,  measurement,  prevention.  Treatment  of  pain  crises. 
Cocain.  Morphin.  Root  section.  General  principles  of 
treating  pain,  gastric,  and  other  crises.  Involuntary  micturi- 
tion :  prevention,  treatment.  Intestinal  and  genital  symp- 
toms. Blindness.  Deafness. 

XIIL— TREATMENT  OF  MOTOR  SYMPTOMS  OF  TABES    .    226 

Faulty  equilibration  first  motor  disorder  in  tabes:  its  meas- 
urement, analysis,  and  prognosis.  Ataxia,  its  prevention 
and  measurement.'  Minimizing  ataxia  by  reducing  move- 
ment and  by  mechanical  supports.  Defects  of  the  tabetic 
foot  as  a  support.  Means  of  ascertaining  and  of  remedying 
these  defects.  New  method  of  obtaining  cast  of  foot  in 
action.  Foot  brace.  Special  tabetic  shoe.  Braces  for  joints. 
Value  of  belt  and  bandages.  Temporary  use  of  all  appli- 
ances. 

XIV.— TREATMENT  OF  DISORDERS  OF  MOVEMENT  IN 

TABES 244 

Removal  of  muscular  constraint.  Easy,  confident,  and  per- 
fect movement  founded  upon  appreciation  of  postural 
images.  Measures  to  insure  appreciation  of  postural 
images.  Blindfolding.  Training  in  attention  and  in  capacity 
for  effort.  The  maintenance  of  optimal  conditions  through- 
out the  treatment.  Training  in  attitude,  recumbent,  sitting, 
"all  fours,"  kneeling,  standing.  Dosage  of  postural  exer- 


CONTENTS  xvii 

CHAPTER  PAGE 

cises.  Training  in  movement  in  these  several  attitudes  as 
they  become  stabilized.  The  cardinal  qualities  of  simple 
movements.  Simple  movements.  Complex  movements. 
Stabilizing  the  base  for  progression.  Progressing.  Creeping. 
Kneeling.  Walking.  Dosage  of  movement  exercises.  Walk- 
ing in  public. 

XV.— REVIEW  OF  TABES 264 

Afferent  nervous  system  invaded  in  disease  styled  tabes 
dorsalis,  or  locomotor  ataxia.  Disturbance  of  vegetative, 
non-vegetative  and  sensory  function.  "Locomotor  ataxia" 
misleading;  "tabes  dorsalis"  useless;  "syphilitic  neuritis  of 
posterior  roots"  suggested.  Diagnosis  and  course  of  inva- 
sion. Division  into  preataxic,  ataxic,  and  paralytic  stages 
a  psychological,  not  anatomical,  division.  Drug  treatment 
of  tabes.  Reciprocal  relations  of  symptoms  and  mental  state 
in  tabes  and  interdependence  of  symptoms.  Treatment  of  the 
symptoms  through  the  mental  state.  Its  ease  and  effective- 
ness. Treatment  of  the  mental  state  through  the  symptoms. 
Former  methods,  Frenkel,  Goldscheider,  Forster.  Limita- 
tions of  Frenkel's  method.  Development  of  present  method. 
Value  of  present  method  in  cure  and  in  prevention.  Con- 
clusion. 

BIBLIOGRAPHY 277 

INDEX  287 


LIST  OF  ILLUSTRATIONS 

FI3.  FAGE 

1. — Spirochetes  in  the  brain  of  a  general  paralytic      ...         3 
2. — The  Spirochaeta  pallida  in  the  brain  of  a  general  paralytic         4 
3. — Spirochaeta  pallida,  from  the  brain  of  a  general  paralytic, 

growing  in    the    testes    of   a    rabbit         ....         6 

4. — Beaussart's  quoted  series       ....  8 

5. — Beaussart's  recorded  series     .......         9 

6. — Diagram  to  show  the  relations  of  the  spinal  cord  and  its 
coverings  to  the  anterior  and  posterior  nerve  roots  and 

to  the  peripheral  nerve 19 

7. — Muscle  spindle  and  motor  end  plate,  diagrammatic       .         .       21 
3. — Tendon   organ,   diagrammatic         .         .  .         .         .21 

9. — Reflex  collaterals  of  posterior  root         .....       22 

10. — Diagram  of  a  simple  reflex  are 

11. — Diagram  of  the  nerve  mechanism  which  correlates  the  action 

of  antagonistic  muscles     .......       25 

12. — Diagram  to  show  a  subminimal  impulse  in  one  reflex  arc 

reinforced  by  a  subminimal  impulse  in  another  reflex  arc       26 
13. — To  show  relations  of  the  sensory  nerves  of  the  musculature 
to  the  cerebellum       ...... 

14. — Graphic  record  of  the  knee  jerk  to  show  its  true  relations       31 
15. — Demonstrating  early  hypotonia  of  the  flexor  muscles  of  the 
knee  of  a  recumbent  tabetic      .... 

16. — Left  genu  recurvatum,  showing  the  importance  of  muscular 

action  in  the  production  of  this  deformity 

17. — Excessive    tabetic    hypotonia         .  .35 

18,19. — Backward  dislocation  of  right  knee  .       36 

20,  21. — Syphilitic  invasion  of  anterior  horn  cells  in  a  tabetic       38 
22. — Chimpanzee's  brain      •.-'       . 
23. — Diagram   showing   the   course,    origin    and   termination    of 

spinal  cord  fibers       ~.         ~i^    • 
24. — The  three  stages  in  the  normal  grasp 
25. — The  tabetic  grasp  showing  asynergia    . 
26.— Anatomical  arrangement  of  the  paths  and  centers  concerned 

in  sensation       .         .         •        • 
27. — Von  Frey's  hairs    ... 
28. — Table  of  von  Frey's  hairs      .         .... 

AQ 

29.— Algesimeter 

30. — Pressure  esthesiometer  for  testing  pressure  touch       .         .       50 


xx  LIST  OF  ILLUSTRATIONS 


PAOE 


31.  —  Modified  Cattell  algometer  for  measuring  pi-essure  pain        .      51 

32.  —  Muscle  spindle       ......        ...      54 

33.  —  Tendon   organ        .........      54 

34.  —  Rufnni's  corpuscle,  from  ligament  of  knee      ....       55 

35.  —  Goldscheider's  instrument   for  measuring  joint   movements       57 

36.  —  "The  mood,  the  emotion,  the  mental  state,  at  the  moment  — 

have  motor  attributes  of  which  we  are  unconscious"      .      63 

37.  —  Tracing  of  lateral  swaying  in  a  normal  person       ...       63 

38.  —  Tripod  stage  of  a  tabetic      .        ......       64 

39.  —  Quadruped  stage  of  a  tabetic       ......      64 

40.  —  Further  development  of  the  "quadruped"  stage        .        .       65 

41.  —  "The  courageous  can  always  maintain,  although  distortedly, 

an  erect  posture"      ........       66 

42.  —  Dr.  Abrahamson's  case  ........      99 

43.  —  Paralysis  of  the  left  third  nerve    ......     105 

44.  —  Complete  paralysis  of  the  fourth  nerve  and  partial  paralysis 

of  the  third       .........     106 

45.  —  Complete  paralysis  of  the  right  sixth  nerve        .        .        .     108 

46.  —  Complete  right  and  partial  left  ptosis  in  tabes      .        .         .    109 

47.  —  Diagrams  to  show  the  effect  of  locomotor  ataxia   on   the 

pupil          .......... 

48.  —  Retraction  of  the  lids,  eccentric  pupils        ... 

49.  —  Tabetic-  with  left  pupil  widely,  right  moderately  dilated 

50.  —  Extirpation  of  Gasserian  ganglion        ..... 

51.  —  Extirpation  of  Gasserian  ganglion        ..... 

52.  —  Extirpation  of  Gasserian  ganglion        ..... 

53.  —  Left  facial  palsy  from  a  basal  fracture        .... 

54.  —  Right  facial  palsy  of  acute  inflammatory  origin 

55.  —  Diagram  showing  relation  of  sympathetic  fibers 

56.  —  Diagram  of  autonomic  or  vagal  and  sympathetic  interaction 

57.  —  Trophic  ulcer  of  the  big  toe        ...... 

58.  —  Trophic  ulcer  of  the  outer  margin  of  the  foot 

59.'  —  Taboparesis    .......        ... 

60.  —  Painless  tabetic  fracture  of  the  head  of  the  tibia 

61.  —  Charcot  left  knee  and  ankle        ...... 

62.—  Tabetic   joints        .        .        .  .      ...... 

63.  —  Charcot  elbow        .  .....        . 

64,  65.  —  Proliferating   osteitis   of   lower   left  'ribs   in    a    tabetic     143 
66.  —  Experimental  brain  syphilis  in  a  rabbit        .        .  .     144 
67.—  The  reckoning  test        .        .        .        .....    1^9 

68.—  The  reckoning  test  of  A.  R.        .        .....    180 

69.—  The  reckoning  test  of  J.  H  .......    181 

70.  —  Description  of  parts  of  pneumograph 

71.  —  Parts  of  recording  apparatus  of  pneumograph     .        .        .     197 

72.  —  Types  of  breathing  disturbance    ......     198 


LIST  OF  ILLUSTRATIONS  xxi 


PAGE 


/  l>. — Types  of  breathing-  disturbance     ......  199 

74. — Types  of  breathing  disturbance     ......  200 

75. — Types  of  breathing  disturbance,  Curve  A       ....  200 

76. — Types  of  breathing  disturbance,  Curve  A  2  .         .         .         .  201 

77. — Types  of  breathing  disturbance,  Curve  A3.         .         .         .  202 

78. — Types  of  breathing  disturbance,  Curve  A  4  .         .         .         .  204 

79. — Types  of  breathing  disturbance,  Curve  A  5  .         .         .         .  205 

80. — Types  of  breathing  disturbance,  Curve  A  6  .         .         .         .  206 

81. — Types  of  breathing  disturbance,  Curve  A  7  .         .         .         .  206 

82. — Chart  of  patient  beginning  treatment,  showing  by  the  reck- 
oning test,  remarkable  improvement  in  her  capacity  for 

simple   mental   tasks 208,209 

83. — Chart  of  gait  in  early  case  of  locomotor  ataxia         .         .  228 

84. — Footprints  in   the   slightly   ataxic 230 

85. — Showing  initial  state  of  a  tabetic 231 

86. — Broad  base  and  crouching  attitude  of  tabetic         .         .         .  232 

87.— Footprints   of   tabetic            233 

88.— Footprints  of  tabetic 234 

89.— Footprints  of  tabetic .        .235 

90.— The  tabetic's  boot 238 

91.— The  tabetic's  boot -  239 

92. — Showing  bandages  used  as  temporary  muscles       .         .         .  240 

93. — Showing  bandages  used  as  temporary  muscles       .         .         .  241 

94.— To  show  effect  of  treatment 241 

95. — To  show  effect  of  treatment 242 

96. — Knee  guards •  257 

97.— To  show  effect  of  treatment  . 274 


LOCOMOTOR  ATAXIA 


CHAPTER  I 

THE  SPIROCHETE  AND  TABES.  THE  SITE  OF  THE  STRUC- 
TURAL CHANGES  PRODUCED  BY  THE  SPIROCHETE  IN 
THE  CENTRAL  NERVOUS  SYSTEM 

Discovery  of  tabes.  Controversy  concerning  its  cause.  Relation  of 
tabes  to  syphilis.  The  Spirochaeta  pallida,  the  exciting  organism 
of  tabes.  Strains  of  spirochete.  Spirochetes  that  persist  in  the 
human  host  and  attack  tissues  usually  immune.  The  three  varie- 
ties of  the  persisting  spirochete.  The  attacking  force  of  the  per- 
sisting spirochete.  Invasion  by  the  pei'sisting  spirochete  of  vascu- 
lar, glandular  and  nervous  tissues.  Causes  which  determine  that 
the  major  attack  shall  fall  upon  the  central  nervous  system.  The 
spirochete's  invasion  not  restricted  to  any  one  area  in  the  central 
nervous  system.  Factors  which  determine  the  initial  site,  the  ex- 
tent and  the  direction  of  the  spirochete  invasion  in  the  central 
nervous  system. 

AFTER  hazy  recognition  by  Todd  (1847)  in  England 
and  by  Romberg  in  Germany  (1841-51),  tabes  was  dis- 
covered by  Duchenne  of  Boulogne  and  its  symptoms 
definitely  separated  from  those  of  other  diseases  in  his 
classical  work  on  "Ataxie  locomotrice  progressive" 
(1857-58). 

Since  Duchenne 's  day,  Charcot,  Dejerine,  Egger,  Four- 
nier,  Pierre  Marie,  Marinesco,  Nageotte  and  Raymond 
in  France;  Erb,  Forster,  Friedrich,  Goldscheider,  Ley- 
den,  Moebius,  Oppenheim,  Striimpell  and  Westphal  in 
Germany ;  Argyll-Robertson,  Byrom  Bramwell,  Graham- 
Brown,  Buzzard,  Ferrier,  Gowers,  Hughlings  Jackson 

and  James  Taylor  in  Britain;  Jelliffe,  Mills,  Noguchi, 

l 


2  LOCOMOTOR  ATAXIA 

Patrick,  Spiller  and  Spitzka  in  America;  Krafft-Ebbing 
and  Schaffer  in  Austria;  and  Frenkel  in  Switzerland, 
have  by  their  genius  and  labor  conferred  upon  us  most  of 
our  present  knowledge  of  tabes. 

The  cause  of  tabes  has  been  the  subject  of  speculation 
and  controversy  almost  from  the  discovery  of  the  dis- 
ease. Erb  and  Moebius  stoutly  upheld  the  syphilitic  ori- 
gin of  tabes.  Fournier  believed  not  only  that  syphilis 
is  the  cause  of  tabes  but  also  that  he  could  gauge  from 
the  nature  of  the  banal  lesions  of  syphilis  the  probability 
of  the  later  occurrence  of  tabes.  Hitzig  taught  that  tabes 
is  due  to  a  toxin  liberated  somewhere  as  the  result  of  ac- 
cident. Others  incriminated  shock,  overwork,  heredity 
and  diverse  causes. 

With  Schaudinn's  discovery  of  the  Spirochaeta  pallida, 
the  protozoon  that  causes  syphilis,  renewed  interest  in 
this  controversy  arose.  Failure  to  find  the  spirochete  in 
the  tabetic  lesion  and  lack  of  success  of  drug  treatment 
directed  against  the  spirochete  in  tabes  led  most  clini- 
cians to  agree  that  tabes  was  due  to  a  toxin.  This  toxin 
was  believed  by  the  majority  to  be  a  by-product  of  the 
spirochete 's  activity;  by  Brissaud  to  be  liberated  from 
the  lymphocytes.  Tabes  free  from  all  taint  of  syphilis 
was  still  thought  to  occur,  and  tabes  not  causally  but  ac- 
cidentally associated  with  syphilis  was  supposed  to  be 
possible. 

Wassermann  proved  that  a  substance  detectable  in  the 
blood  and  in  the  cerebrospinal  fluid  may  result  from  in- 
fection by  the  Spirochaeta  pallida.  Its  presence  practi- 
cally signifies  syphilis  but  its  absence  does  not  preclude 
syphilis.  Mclntosh  and  Fildes  found  the  "Wassermann 
substance  in  the  cerebrospinal  fluid  of  over  ninety  per 
cent,  and  Hauptmann  and  Nonne  in  one  hundred  per 


THE  SPIROCHETE  AND  TABES 


cent,  of  cases  of  tabes.    Spirochete  infection  is,  therefore, 
an  invariable  accompaniment  of  tabes.    There  is  no  tabes 
without  syphilis. 
Vedder  ascertained  by  blood  examination  that  seven- 


FIG.  1. — Spirochetes  in  the  brain  of  a  general  paralytic.     (Noguchi.) 

teen  per  cent  of  the  recruits  of  the  United  States  Army 
are  syphilitic.    As  syphilis  occurs  only  in  seventeen  per 
cent  of  the  non-tabetic  and  in  one  hundred  per  cent  of  the 
tabetic,  syphilis  has  a  causal  relation  to  tabes. 
In  tabes  a  degeneration  .of  the  nerve  processes  and  a 


LOCOMOTOR  ATAXIA 


proliferation  of  the  cells  of  the  blood  vessels  and  of  the 
stroma  occur.  These  lesions  are  of  a  nature  compatible 
with  syphilitic  origin. 

Pathologists  now  recognize,  at  the  starting  point  of 


' 

I 


FIG.  2. — The  Spirochaeta  pallida  in  the  brain  of  a  general  paralytic.   X  1 100. 

(Noguchi.) 

every  tabetic  change,  an  exudative  focus.    Exudates  are 
evidence  of  inflammatory,  not  of  toxic,  action. 

In  the  tabetic  exudate  Noguchi  and  others  found  the 
spirochete  viable  and  culturable. 


THE  SPIROCHETE  AND  TABES  5 

No  organism  other  than  the  spirochete  has  been  found 
in  the  inflammatory  foci  of  tabes. 

As  syphilis  is  invariably  present  in  tabes,  as  syphilis 
has  a  causal  relation  to  tabes,  as  the  lesions  of  tabes 
are  such  as  could  be  produced  by  the  spirochete,  as  the 
spirochete  has  been  detected  in  the  tabetic  lesions,  and  as 
it  is  the  only  known  organism  which  has  this  constant 
association  with  tabes,  the  Spirochaeta  pallida  must  be 
the  exciting  organism  of  tabes. 

The  Wassermann  substance  can  be  detected  in  the  blood 
a  few  weeks  after  the  primary  inoculation :  according  to 
Wile  and  Stokes,  Nichols  and  others,  the  majority  of  the 
cases  of  syphilis  in  the  secondary  stage  and  many  in  the 
primary  stage  show  evidence  of  the  infection  in  the  cere- 
brospinal  fluid  also.  The  local  inoculation  with  syphilis, 
therefore,  early  becomes  a  general  infection. 

When  the  infection  is  general  the  tissues  are  equally 
accessible.  The  tissue  first  attacked  must,  therefore,  be 
that  which  affords  the  most  favorable  soil  for  the  spiro- 
chete 's  growth.  The  skin  and  the  mucous  membranes  are 
the  contact  surfaces  of  human  beings.  From  the  skin 
and  mucous  membrane  lesions  of  one  host  originate  le- 
sions of  the  skin  and  mucous  membranes  of  another  host. 
The  most  frequent  and  often  the  only  sign  of  the  family 
taint  in  the  wife  and  child  of  a  tabetic  or  of  a  general 
paretic  is  a  lesion  of  the  nervous  mechanism  of  the  pupil ; 
from  a  spirochete  growing  in  the  nervous  system  of  one 
host,  a  spirochete  growing  only  in  the  nervous  system  of 
another  host  may  result.  The  spirochete  in  a  new  host 
grows  best  in  the  tissue  from  which  it  is  derived.  The 
strain  of  spirochete  is  somewhat  specific  for  the  tissue  it 
invades,  for  the  tissue  in  which  it  grows.  McDonagh 
and  Ross  state  that  these  strains  may  be  morphologically 


LOCOMOTOR  ATAXIA 


differentiated;  except  variations  in  viability  and  in  the 
rate  of  growth  in  cultural  media,  no  definitely  distinctive 
characteristics  have  been  found  by  other  observers,  in- 
cluding Noguchi,  Nichols,  and  Reasoner,  to  separate 
these  strains. 


FIG.  3. — Spirochaeta  pallida  from  the  brain  of  a  general  paralytic  growing 
in  the  testis  of  a  rabbit.     (Noguchi.) 

When  a  person  acquires  a  spirochete  from  contact  with 
skin  or  mucous  membrane  lesions,  the  infection  soon  be- 
comes general  and  shortly  thereafter  lesions  appear  in 
that  person's  skin  and  mucous  membranes,  heal  and  re- 


THE  SPIROCHETE  AND  TABES  7 

cur ;  but  till  the  last  has  finally  healed,  none  as  a  rule  is 
seen  in  the  deeper  tissues. 

When  the  emasculated  and  less  numerous  spirochetes 
invade  the  deeper  tissues,  lesions  occur  there  but  not 
elsewhere :  the  gumma  develops  alone,  unaccompanied  by 
either  skin  or  mucous  membrane  lesions  or  by  lesions  of 
the  central  nervous  system.  So  well  recognized  is  this 
incidence  that  the  rare  lesions  which  contravene  the  rule 
are  styled  precocious.  The  central  nervous  system  le- 
sions do  not  occur  together  with  lesions  of  the  deep  tis- 
sues, nor  of  the  skin  and  mucous  membranes.  Spillman 
and  Perrin  have  reported  the  occasional  occurrence  of 
gummata  and  even  of  cutaneous  syphilids  with  tabes 
and  writh  general  paresis ;  but  such  rare  happenings  serve 
merely  to  emphasize  the  rule  that  only  one  type  of  tis- 
sue is  attacked  at  a  time. 

Few  syphilitics  enter  matrimony  ere  the  skin  and  mu- 
cous membrane  lesions  heal.  The  healthy  partner  is  in- 
fected by  a  spirochete  already  repelled  from  the  skin 
and  mucous  membranes  of  the  infecting  partner,  a  spiro- 
chete which  can  grow  with  difficulty  or  not  at  all  in  the 
skin  and  mucous  membranes  of  the  new  host.  The  mild- 
ness of  the  skin  and  mucous  membrane  lesions  in  con- 
jugal syphilis  is  notorious.  The  spirochete  of  the  gumma 
and  of  the  tabetic  lesion  so  rarely  produce  skin  and 
mucous  membrane  lesions  in  another  host,  that  tertiary 
and  nervous  lesions  are  commonly  considered  to  be  non- 
infective. 

The  spirochete  to  which  a  particular  tissue  or  tissues 
in  one  host  have  achieved  immunity  loses  the  power  to 
attack  that  tissue  or  tissues,  not  only  in  the  host  where 
the  successful  defense  occurred,  but  also  in  any  other 
host,  probably  to  the  extent  to  which  the  biochemical  re- 


8  LOCOMOTOR  ATAXIA 

actions  of  the  same  tissues  in  the  two  hosts  are  identical. 
The  spirochete  acquires  in  the  human  host  characters 
which  enable  it  to  grow  best  in  a  certain  tissue.  If  that 
tissue  be  the  skin  and  mucous  membranes,  the  spirochete, 
after  growth  there,  may  grow  in  the  deeper  tissues ;  and, 
still  later,  in  the  central  nervous  system.  If  that  tissue 
be  not  the  skin  and  mucous  membranes,  then  the  spiro- 
chete's  growth  is  impossible  there,  but  is  possible  in  the 
deeper  tissues,  and  later  in  the  central  nervous  system. 
If  that  tissue  be  the  central  nervous  system  the  spiro- 
chete may  grow  best  and  only  there. 

D 

Hus  band 


First  Wife 


-•Second  Wife 


Daughter 

FIG.  4. — Beaussart's  quoted  series.     D,  Non-nervous  syphilis;  •,  syphilis 
of  the  central  nervous  system. 

One  strain  of  spirochete  which  may  produce  tabes  is 
a  spirochete  which  can  grow  best  or  only  in  the  central 
nervous  system;  a  spirochete  which  is  derived  from  a 
host  in  whom  it  has  been  successfully  repelled  from  the 
skin  and  mucous  membranes  and  deeper  tissues ;  a  spiro- 
chete which  causes  tabes  after  no  or  slight  pretabetic 
lesions,  a  spirochete  which  is  partly  blamable  for  the 
many  cases  of  tabes  that  are  ignorant  of  their  infection, 
and 'for  the  long  accepted  but  erroneous  belief  that  tabes 
can  develop  without  syphilitic  infection. 

Belieres  records  three  cases  of  general  paresis  and 
two  of  an  allied  nature  that  all  owed  their  infection  to 


THE  SPIROCHETE  AND  TABES 


the  same  woman.  Beaussart  quotes  a  series  in  which  a 
syphilitic  husband,  free  from  nervous  affection,  had  a 
wife  who  became  tabetic,  and  a  daughter  who  was  a  gen- 
eral paretic.  After  divorce,  the  husband  remarried  and 
his  second  wife  also  developed  tabes. 

Beaussart  records  a  series  in  which  a  glassblower,  X., 
acquired  a  buccal  chancre  from  a  drinking  cup  used  by 
a  fellow  workman,  Y.  X.  and  his  wife  died  of  general 

Y'sTWife 


Y's  Wife's  Paramour 


X's  Wife 

FIG.  5. — Beaussart's    recorded    series.     O,   Non-nervous   syphilis;  •,    •  , 
syphilis  of  the  nervous  system. 

paresis.  Y.  died  of  general  paresis.  Y.'s  wife  remained 
normal  but  her  paramour  developed  tabes. 

Beaussart  mentions  a  man  who  became  a  general  pare- 
tic and  whose  wife  showed  taboparesis :  her  lover  devel- 
oped general  paresis  and  his  wife  had  syphilitic  pupil- 
lary changes.  Morel  Lavallee  records  five  cases  of  gen- 
eral paresis,  and  Erb  five  cases  of  tabes,  with  a  common 
source  of  infection.  Pierre  Marie  and  Bernard  and  oth- 
ers have  reported  similar  groups. 

In  such  groups  no  single  source  of  infection,  far  less 
an  unique  exposure  to  syphilis,  can  be  established.  Yet 


10  LOCOMOTOR  ATAXIA 

the  larger  the  group  or  series  of  similarly  affected  cases 
the  greater  is  the  probability  that  their  common  experi- 
ence is  also  the  source  of  their  common  mischance. 
From  a  common  source  organisms  of  an  uniform  viru- 
lence are  derived.  If  in  spite  of  possible  differences  in 
dose,  in  treatment,  and  in  defense,  a  series  of  persons 
infected  from  a  common  source  acquire  nervous  symp- 
toms, either  a  spirochete  with  a  particular  faculty  to  in- 
vade nerve  tissue  is  the  infecting  agent,  or  several  per- 
sons, reacting  to  the  ordinary  spirochete  in  the  same  ex- 
traordinary way,  are,  by  a  remarkable  coincidence,  in- 
fected from  the  same  source. 

Belieres'  report  makes  no  mention  of  nervous  affec- 
tion in  the  woman  alleged  to  have  transmitted  the  taint ; 
in  Morel  Lavallee's  series  the  alleged  source  of  infection 
did  not  herself  suffer  from  syphilis  of  the  nervous  sys- 
tem; in  Beaussart's  recorded  series,  Y.'s  wife  had  no 
implication  of  the  nervous  system.  To  establish  the  ex- 
istence of  a  special  strain  of  spirochete  which  can  tri- 
umph over  the  average  human  resistance  and  finally  at- 
tack the  nervous  system,  it  is,  however,  not  necessary 
for  all  exposed  to  that  spirochete  to  develop  syphilitic 
nervous  lesions.  If  in  one  series  of  syphilitics  the  pro- 
portion of  cases  of  nervous  disease  is  greater  than  the 
usual  proportion  in  which  nervous  disease  follows  syph- 
ilis, then  a  special  strain  may  be  acting  in  that  series. 

A  second  analogous  series  weakens  the  possibility  that 
persons  reacting  to  spirochete  infection  in  the  same  un- 
usual manner  were  coincidently  infected,  at  the  same 
source,  by  an  ordinary  spirochete,  and  increases  the 
probability  that  the  reaction  which  characterized  the 
series  is  due  to  a  special  invasive  power  of  the  spiro- 
chete infecting  them  in  common.  Every  additional  series 


THE  SPIROCHETE  AND  TABES  11 

immeasurably  enhances  this  probability.  Even  the  few 
I  have  cited  demonstrate  that  there  are  one  or  more 
strains  of  the  spirochete  which  characteristically  per- 
sist in  spite  of  the  average  human  resistance,  which  at- 
tack the  nervous  system,  and  which  maintain  this  power 
of  attack  in  transmission  from  host  to  host.  Perhaps 
the  person  in  any  group  free  from  nervous  lesions  is 
the  original  source  of  the  group  infection. 

The  persisting  spirochete  is  one  which  can  overpower 
the  average  human  resistance ;  or  one  which,  being  of  av- 
erage virulence,  encounters  subnormal  resistance ;  or  one 
which  evades  the  usual  resistance  by  its  inability  to  at- 
tack the  outpost  tissues. 

The  persisting  spirochete  has  an  attacking  force  which 
depends  upon  its  numbers  and  virulence.  With  this  force 
the  persisting  spirochete  attacks  tissues  which  are 
usually  safeguarded.  Among  these  protected  tissues  the 
central  nervous  system  does  not  suffer  alone ;  the  cardio- 
vascular and  glandular  systems  are  also  invaded.  The 
cardiovascular  system  is  invariably  attacked:  the  attack 
is  usually  ignored  because  of  the  more  bizarre  and  insist- 
ent results  of  the  concomitant  nervous  lesions.  But 
many  authors  have  emphasized  the  frequency  of  cardio- 
vascular, especially  aortic,  lesions  in  tabes;  Matsunaga 
found  fifteen  cases  of  cardiac  disease  among  ninety-nine 
tabetics.  Burr,  Grossman,  and  others  have  shown  the 
importance  of  cardiovascular  and  renal  lesions  in  bring- 
ing death  to  the  tabetic.  Striimpell  has  demonstrated  the 
frequency  with  which  patients  suffering  from  aortic  and 
other  vascular  lesions  of  syphilitic  origin  show  signs, 
such  as  fixed  pupils  and  loss  of  tendon  reflexes,  of  con- 
comitant syphilitic  affection  of  the  central  nervous 
system. 


12  LOCOMOTOK  ATAXIA 

Strains  of  spirochete  which  grow  best  in  the  central 
nervous  system;  poisons,  such  as  alcohol  and  tobacco, 
which  lower  the  vitality  of  the  nerve  elements ;  and  con- 
stitutional, environmental  and  occupational  influences 
which  render  the  nervous  the  most  vulnerable  system, 
are  the  factors  that  decide  that  the  major  attack  of  the 
persisting  spirochete  shall  fall  on  the  nervous  system. 

Attacking    force    of 
Liability  to  syphilis  of  spirochete 


central  nervous  system  = 


Inherited  +  acquired 
resistance. 


In  the  central  nervous  system  the  spirochete  has  no 
exclusive  site  of  attack. 

At  least  ten  per  cent  of  tabetics  show  optic  atrophy. 
Galezowski  found  posterior  root  lesions  in  717  out  of 
1029  optic  atrophies.  Mott  states  that  fifty  per  cent  of 
cases  of  syphilitic  optic  atrophy  end  in  general  paresis. 
Tabes  may  change  to  general  paresis.  Dejerine  states 
that  more  than  half  the  cases  of  general  paresis  show 
signs  of  implication  of  the  posterior  roots. 

The  syphilitic  invasion  called  tabes  may  advance  till 
much  of  the  central  nervous  system  is  implicated. 

Oppenheim  found  in  all  of  the  fourteen  cases  of  tabes 
which  he  examined  endoneuritis  or  perineuritis  in  the 
peripheral  sensory  nerves.  There  may  be  one  or  several 
foci  in  a  nerve.  Such  foci  may  occur  in  the  secondary 
stage  of  syphilis  and  may  not  be  followed  by  tabes.  Each 
focus  may  implicate  few  or  many  fibers.  The  resulting 
destruction  is  usually  partial  and  often  insignificant. 
Nonne  and  others  have  examined  cases  in  which  they 
failed  to  find  lesions  in  the  peripheral  nerves. 

Jendrassik,  who  had  a  cerebral  theory  of  ataxia  to  sub- 
stantiate, declared  that  a  special  area  of  the  cerebral 


THE  SPIROCHETE  AND  TABES  13 

cortex  was  characteristically  implicated  in  tabes.  Le- 
sions all  over  the  cortex  have  been  since  reported.  Gen- 
eral paresis  may  early  or  late  supervene  in  tabes.  Gor- 
don Holmes  has  shown  that  tabes  may  occur  without  any 
cortical  lesions. 

The  oculomotor  and  abducens  nerves  are  usually  af- 
fected, less  often  the  trochlear;  the  vagus  much  more 
frequently  than  the  fifth;  but  all  the  cranial  nerves  have 
been  found  implicated  both  in  their  course  and  in  their 
nuclei  of  origin. 

Together  with  the  vestibular  branches  of  the  eighth, 
and  independently,  the  cerebellum  may  be  attacked. 

Not  only  the  vagal  but  also  the  sympathetic  component 
of  the  vegetative  nervous  system  may  be  extensively  dis- 
eased in  tabes.  Of  the  sympathetic  fibers  those  in  the 
posterior  roots  are  usually  attacked.  The  dorsal  sympa- 
thetic, as  a  rule,  suffers  first  and  most. 

Tabetic  foci  have  been  seen  in  the  anterior  horn  cells 
as  well  as  among  their  homologues  in  the  basal  nuclei. 
Such  foci  are  rare  and  occur  late.  S.  A.  K.  Wilson  states 
that  they  are  accidental  complications  of  tabes.  Lesions 
in  motor  nerves  have  also  been  occasionally  observed. 

Homen  and  Marinesco  demonstrated  the  presence  of 
the  spirochete  in  the  lymphatic  channels  of  peripheral 
nerves.  Orr  and  Rows  showed  that  a  communication  ex- 
ists between  the  general  and  the  cerebrospinal  lymphatic 
systems,  at  the  posterior  nerve  roots;  and  that  a  con- 
tinuous upward  flow  of  lymph  occurs  along  the  periph- 
eral nerves  and  through  the  posterior  roots.  Hence 
the  invasion  of  the  posterior  roots  was  attributed  to  their 
accessibility  to  the  spirochete.  Poirier  found  a  similar 
communication  in  the  optic  nerve  sheath  which  seemed 
to  explain  the  liability  of  the  optic  nerve  to  invasion. 


14  LOCOMOTOR  ATAXIA 

But  in  the  olfactory  sheath,  also,  there  exists  such  a 
communication :  another  is  present  in  the  eighth  nerve 
sheath ;  and  still  others  exist  where  tabetic  lesions  are  in- 
frequent. As  the  spirochete  invasion  early  becomes  gen- 
eral; as  sites  which  enjoy  with  the  posterior  roots  and 
optic  nerves  a  communication  between  the  general  and 
the  cerebrospinal  lymphatic  systems  do  not  share  with 
these  an  equal  liability  to  attack  by  the  spirochete;  and 
as,  moreover,  Guillain  and  others,  by  injection  of  color-, 
ing  matter,  have  demonstrated  a  constant  circulation  oc- 
curring in  the  cerebrospinal  lymphatic  system,  the  dis- 
tribution of  the  spirochete  probably  plays  an  insignifi- 
cant role  in  determining  the  site  of  the  initial  attack. 

The  main  stress  of  ergot  poisoning  falls  on  the  pos- 
terior roots;  of  amyl  alcohol  on  the  optic  nerve;  of 
strychnin  and  of  tetanus  toxin,  probably,  on  the  synapse 
of  the  anterior  horn  cell.  Only  local  differences  in  the 
chemical  composition  of  the  nervous  system  can  account 
for  the  selection  by  these  several  poisons  of  their  respec- 
tive sites.  Such  chemical  differences  may  render  cul- 
tural conditions  at  one  site  favorable,  at  another  site  less 
favorable,  to  the  growth  of  organisms. 

Some  cells,  owing  to  developmental  characteristics, 
may  be  less  resistant  than  others ;  cells  whose  processes 
are  unprotected  by  a  neurilemmal  sheath  may  be  more 
vulnerable  than  others  which  are  sheathed. 

Edinger  fatigued  rats  by  placing  them  on  a  con- 
tinuously moving  treadmill.  He  then  poisoned  them 
with  pyridin  and  found  the  lesions,  although  dissemi- 
nated, mainly  in  the  posterior  root  zones.  In  Professor 
Kraepelin's  laboratory,  one  eye  of  certain  rodents  was 
closed.  The  open  eye  was  then  exhausted  by  bright 
flashes  of  light,  recurring  every  minute,  for  several 


THE  SPIROCHETE  AND  TABES  15 

weeks.  After  injecting  amyl  alcohol  into  these  rodents, 
one  found  the  optic  nerve  of  the  open  eye  showed  greater 
destruction  than  that  of  the  closed.  It  has,  therefore, 
been  proved  that  nerve  elements  exhausted  by  excess  of 
functional  activity  resist  less  than  unfatigued  nerve 
cells,  the  action  of  toxic  agents.  We  may  infer  that  neu- 
rons exhausted  by  over-function  resist  less  than  those 
not  so  fatigued,  invasion  by  organisms. 

The  amount  of  stress  to  which  a  neuron  is  subjected 
depends  upon  its  function  and  upon  its  owner's  environ- 
ment. The  functioning  of  sensory  neurons,  particularly 
of  those  which  constitute  the  posterior  roots,  is  almost 
incessant;  whereas,  that  of  motor  neurons  is  intermit- 
tent. Sensory  neurons  are  commonly,  motor  rarely,  at- 
tacked by  the  spirochete. 

Only  unconvincing  evidence  has  been  yet  offered  to 
prove  the  influence  of  occupation  in  determining  the  site 
of  the  initial  lesion,  for  neurologists  have,  as  a  rule,  con- 
founded disability  due  to  psychic,  with  that  due  to  struc- 
tural, causes.  But  Hitzig,  Oppenheim,  and  others  have 
emphasized  that  among  the  posterior  roots  those  of  an 
injured  limb  are  first  attacked;  and  the  frequency  with 
which  the  vagal  and  the  sympathetic  components  of  the 
vegetative  nervous  system  are  over-stimulated  from  the 
mental  stress  which  conduces  to  tabes  may  explain  why 
these  components  are  so  often  found  degenerated  in  tabes. 

"Where  the  spirochete  finds  the  most  favorable  soil  in 
which  to  grow  and  the  lowest  resistance,  it  commences 

the  invasion. 

Attacking  force  of  spirochete. 

Liability  of  a  neuron  to  invasion  = 

Defensive  power  of  neuron. 

When  an  optic  nerve  is  attacked,  that  optic  nerve  is  at 
the  moment  of  invasion  less  capable  of  defense  than  the 


16  LOCOMOTOR  ATAXIA 

other  optic  nerve,  than  the  spinal  roots,  than  the  cere- 
bral cortex  and  than  any  other  site. 

When  two  sites  in  the  same  nerve,  or  in  different 
nerves;  two  optic  nerves;  two  spinal  roots;  an  optic 
nerve  and  a  spinal  root,  are  equally  vulnerable  they  are 
simultaneously  attacked. 

When  the  attack  shifts,  it  shifts  to  the  next  most  vul- 
nerable site.  It  is  noteworthy  that  when  the  disease 
starts  in  one  optic  nerve,  the  next  site  attacked  is  usually 
the  other  optic  nerve.  Similarly,  when  the  posterior 
roots  are  first  attacked  the  disease  tends  to  spread  among 
posterior  roots  in  preference  to  other  sites. 

If  the  optic  nerve  be  the  first  attacked,  the  lesions  there 
are  usually  more  severe  than  if  the  optic  follow  spinal 
lesions. 

Perhaps  the  spirochetes  acquire  a  predilection  for  sites 
chemically  identical  with  those  wherein  they  first  success- 
fully grow  in  the  nervous  system;  But  sometimes  the 
attack  halts  in,  say,  the  spinal  roots,  and  begins  in  the 
optic  nerve;  the  resistance  of  the  optic  nerve  then  has 
fallen  lower  than  that  of  the  spinal  roots. 

In  the  central  nervous  system,  as  in  other  tissues,  the 
lesions  of  syphilis  tend  to  appear  in  crops  separated  by 
periods  of  outwardly  perfect  quiescence. 

After  a  completely,  or  incompletely,  successful  attack 
on  the  posterior  roots  or  on  the  optic  nerves,  no  further 
lesions  may  occur.  Then  the  spirochete  either  has  per- 
ished or  has  been  rendered  finally  quiescent:  competent 
seekers  have  so  far  failed  to  find  the  spirochete  in  the 
optic  lesions.  If  no  other  spirochetes  exist  active  in  that 
host,  the  spinal  roots  are  spared  attack.  In  this  sense, 
and  only  in  this  sense,  does  optic  tabes  arrest  spinal 
tabes,  does  spinal  tabes  arrest  optic  tabes.  The  pres- 


THE  SPIROCHETE  AND  TABES  17 

ence-  or  absence  of  lesions  in  the  optic  nerve  or  at  any 
other  site  in  no  way  renders  other  sites  more  fragile  or 
more  resistant.  Optic  atrophy  has  no  more  influence  in 
arresting  spinal  tabes  than  has  general  paresis. 

With  one  exception,  which  we  shall  later  (page  50) 
consider,  the  site  first  attacked  is  usually  the  chief  site 
of  the  disease,  but  the  longer  the  invasion  lasts  the  less 
the  primary  tends  to  be  the  sole  site. 

Much  labor  has  been  expended  in  determining  the  fre- 
quency with  which  various  sites  are  exclusively  and  in 
their  combinations  attacked.  Such  frequency  may  vary 
widely.  Thus,  Dejerine  states  that  muscular  atrophy 
occurs  in  20  per  cent  of  cases  of  tabes:  Duchenne,  in  8 
per  cent  and  Eulenberg,  in  0.6  per  cent.  Each  of  these 
percentages  is  doubtless  correct,  but  only  for  the  par- 
ticular group  of  cases  examined  by  its  observer.  Deje- 
rine's  group  comprised  many  cases  of  long  standing; 
Eulenberg 's  comprised  many  recent;  hence  their  statis- 
tics differ. 

There  is  no  spirochete  which  can  attack  only  the  pos- 
terior root,  or  only  the  cortex  and  not  other  sites  in  the 
central  nervous  system.  By  the  symptoms  which  are 
dominant  we  clinically  identify  the  syphilitic  invasion; 
and  the  disease  conserves  its  identity  just  so  long  as  this 
dominance  is  maintained. 


CHAPTER  II 
RESULTS  OF  THE  SYPHILITIC  LESIONS 

1.  DISTURBANCE  OF  THE  REFLEX  MOTOR  FUNCTION 

The  posterior  root  ganglion  and  coverings.  Ganglion  cell  lesions. 
Meningeal  lesions.  The  posterior  root  itself  a  primary  site  of 
spirochete  invasion.  Nature  and  result  of  the  syphilitic  change 
in  the  posterior  root.  The  sensory  nerve  of  muscle.  The  simple 
reflex  arc  of  muscle  tone.  The  functional  linking  of  reflex  arcs. 
The  knee-jerk;  its  relation  to  the  reflex  arc  of  muscle  tone;  its 
governing  factors.  Alterations  of  tendon  reflexes  in  tabes.  Hy- 
potonia :  effect  on  strength  and  mobility  of  joints.  Dislocations. 
Contortions.  Muscular  weakness  of  tabes;  causes.  Disintegra- 
tion of  reflex  function.  Influence  of  extent,  rapidity,  site  and 
duration  of  the  lesion.  Measurement  of  the  amount  of  the  dis- 
turbance. Identical  motor  effects  produced  by  reflex  and  by  cor- 
tical action.  Site,  paths  and  nature  of  cerebral  control  of  move- 
ment. Reflex  defects  masked  during  voluntary  movement. 

THE  spinal  cord  is  built  of  segments  each  of  which 
possesses  an  anterior  and  a  posterior  root.  On  every 
posterior  root  is  a  mass  of  nerve  cells,  called  a  spinal 
ganglion.  Every  cell  of  a  spinal  ganglion  is  bipolar; 
that  is,  has  two  processes,  a  peripheral  and  a  central. 
The  peripheral  processes  constitute  the  common  sen- 
sory nerves,  and  in  skin,  muscle,  tendon,  cartilage  and 
other  tissues  terminate  as  specialized  sense  organs,  called 
receptors. 

The  central  processes,  passing  to  the  spinal  cord,  con- 
stitute the  greater  part  of  the  posterior  nerve  root.  The 
posterior  nerve  root  is  covered  by  a  prolongation  of  the 
meningeal  covering  of  the  spinal  cord. 

In  tabes  the  bipolar  cells  of  the  spinal  ganglion  have 

18 


EESULTS  OF  SYPHILITIC  LESIONS 


19 


been  seen  in  all  stages  of  disintegration.  The  cell  changes 
may  be  primary  or  may  be  secondary  to  lesions  in  their 
peripheral  or  in  their  central  processes.  A  lesion  of  its 
peripheral  process  produces  more  profound  changes  in 
a  bipolar  cell  than  a  lesion  of  its  central  process.  Changes 
in  the  bipolar  cells  are  seldom  extensive  and  may  indeed 
be  undetectable  (Schaffer). 


SPINAL  6AHGUON 

ON 
POSTERIOR  ROOT 


POSTERIOR 

ROOT 
HCNING-EAL  COVERING  OF  POSTERIOR  ROOT 


COLUMN 
Of 

BURD/ICH 


COLUMN 

or 

&OLL 


PERIPHERAL  N£*V£ 
PARTLY  MOTOR- PARTLY  SfHSOKY 

FIG.  6. — Diagram  to  show  the  relations  of  the  spinal  cord  and  its  coverings 
to  the  anterior  and  posterior  nerve  roots  and  to  the  peripheral  nerve. 

The  meningeal  coverings  of  the  posterior  roots  may 
be  opaque  and  thickened  and  the  meninges  elsewhere 
normal.  More  commonly,  the  thickening  spreads  to  the 
spinal  cord  where  scattered  patches  of  chronic  menin- 
gitis may  also  occur,  especially  in  advanced  cases.  But 
the  meninges  may  be  unaffected. 

Pierre  Marie  attributed  the  degeneration  of  the  pos- 
terior root  fibers  in  tabes  to  the  destruction  of  the  bi- 


20  LOCOMOTOR  ATAXIA 

polar  cells  from  which  they  originate  in  the  spinal  gan- 
glion. But  as  the  earliest  degeneration  in  the  posterior 
root  is  more  extensive  remote  from,  than  near  to,  the 
spinal  ganglion,  the  degeneration  of  the  posterior  root 
fibers  is  not  a  consequence  of  the  destruction  of  the  gan- 
glion cells.  Indeed,  degeneration  of  the  posterior  roots 
not  rarely  is  unaccompanied  by  any  spinal  ganglion  le- 
sions. 

Others  have  stated  that  degeneration  of  the  posterior 
root  fibers  is  a  result  of  an  inflammation  of  the  root's 
coverings.  The  site  of  the  greatest  degeneration  is 
usually  not  in  the  fibers  immediately  under  the  meninges. 
Severe  meningitis  may  be  associated  with  slight  degen- 
eration of  the  root  fibers;  severe  degeneration  may  be 
associated  with  slight  meningitis  or  even  with  no  menin- 
gitis. Hence  posterior  root  degeneration  may  occur  in- 
dependently of  meningitis. 

The  posterior  root  lesion  may  occur  in  absence  of  le- 
sions in  the  spinal  ganglion  and  in  the  meninges.  The 
posterior  root  is,  therefore,  a  primary  site  of  syphilitic 
invasion.  This  initial  posterior  root  lesion  may  be  aug- 
mented from  foci  appearing  synchronously  or  subse- 
quently in  the  spinal  ganglion  or  in  the  meninges.  The 
meninges  and  the  spinal  ganglion  cells  may  be  affected 
independently  of,  or  secondarily  to,  the  posterior  root. 

The  reaction  in  the  posterior  root  to  the  spirochete 
invasion  is  not  solely  a  degeneration  of  nerve  fibers. 
Here,  as  elsewhere  in  the  body,  no  organismal  attack  on 
the  essential  cells  can  occur  without  a  defensive  response 
in  their  supporting  tissue.  In  the  stroma  which  sup- 
ports the  nerve  fibers,  the  lymphocytes  and  mast  cells 
congregate  around  the  attacked  focus,  the  fixed  tissue 
cells  multiply,  and  the  endothelium  proliferates  in  the 


EESULTS  OF  SYPHILITIC  LESIONS 


21 


vascular  and  lymphatic  channels.  Indeed,  Nageotte, 
from  careful  studies,  concludes  that  the  change  in  the 
posterior  root  is  a  transverse  interstitial  neuritis.  Fur- 


FIG.  7. — Muscle  spindle  (left)  and  motor  end  plate  (right),  diagrammatic. 
(Regaud,  Graham  Brown.) 

ther  histological  examination  with  the  Nissl  methods 
perfected  by  Alzheimer  are  needed  to  confirm  or  dis- 
prove Nageotte 's  conclu- 
sion; but  such  examinations 
in  the  optic  nerve  in  tabes 
have  shown  the  change  to 
affect  primarily  the  nerve 
processes  and  secondarily 
the  interstitial  tissue  ( Star- 
gar  dt). 

Beginning  probably 
among  the  middle  zone  fibers 
(Schaffer),  the  syphilitic  in- 
vasion spreads  to  affect 
other  fibers  of  the  posterior 
root.  Roots  may  be  attacked 
simultaneously  or  in  succes- 
sion. The  disease  is  said  to 
begin  usually  in  the  lumbo- 

sacral  roots,  sometimes  unilaterally,  as  a  rule  bilaterally. 
It  spreads  early  to  the  dorsal,  later  to  the  cervical,  roots. 


I< 


FIG.  8. — Tendon    organ, 
matic.  (Regaud, 

Brown.) 


diagram- 
Graham 


22 


In  these  regions  it  advances,  most  destruction  occurring, 
commonly,  in  the  lumbodorsal  region.  One  or  several  or 
the  majority  of  the  posterior  roots  in  a  region  may  be 
implicated.  A  root  may  be  wholly  destroyed ;  generally 
some  of  its  fibers  escape.  A  fiber  may  have  one  or  more 
diseased  foci. 

Every  fiber  of  the  pos- 
terior nerve  root,  which  is 
a  central  process  of  a  bi- 
polar cell  of  a  spinal  gan- 
glion, wThen  it  reaches  the 
cord,  divides  into  two 
main  branches,  an  ascend- 
ing and  a  descending ;  and 
these  give  off  many  lat- 
eral twigs  called  collat- 
erals. 

A  syphilitic  lesion  in 
the  posterior  root  may 
sever  this  central  process. 
On  the  peripheral  side  of 
such  a  lesion  a  fragment 
of  the  central  process  is  left  attached  to  the  ganglion 
cell :  but  the  greater  part,  lying  on  the  spinal  side  of  the 
lesion,  is,  with  all  its  branches,  then  cut  off  from  its 
cell  of  origin,  its  center  of  nutrition  in  the  spinal  gan- 
glion; and,  in  consequence,  degenerates.  Degeneration 
occurs  simultaneously  throughout  the  severed  portion, 
stem,  branches  and  twigs. 

The  sensory  nerve  of  voluntary  muscle  originates,  as 
the  other  sensory  nerves  do,  in  a  bipolar  cell  (a2,  Fig.  10), 
in  a  spinal  ganglion,  on  a  posterior  nerve  root.  The  pe- 
ripheral (a1,  Fig.  10)  of  the  two  fibers  of  this  cell  ends 


FIG.  9. — Reflex  collaterals  of  posterior 
root  (Lenhossek,  Graham  Brown.) 


RESULTS  OF  SYPHILITIC  LESIONS 


23 


within  a  muscle  as  a  fusiform  structure  which  is  called 
a  muscle  spindle  (a,  Fig.  10).  The  central  fiber  passes 
along  the  posterior  nerve  root,  to  the  posterior  zone  of 
the  spinal  cord,  where  it  gives  off  a  lateral  branch,  the 
reflex  collateral  (a5,  Fig.  10).  This  reflex  collateral  tra- 
verses the  gray  matter  of  the  cord,  from  the  posterior 
horn  to  the  anterior,  to  form  a  junction  called  a  synapse, 
with  a  nerve  cell  there  (a6,  Fig.  10). 


0,J  T/)8ET/C  LESJON  W  CENTRAL 
PROCESS  OF  BIPOLAR  CELL 


POSTER/OK  K.OOT 


\T     MOTOR.  C£LL  Of 
\    ANTERIOR  HORN,   ^ 
PEK/PH£R/)L\P/?OC£SS  *' 


•  POSTER/OR  ROOT 
POSTER /OR  HORN 


ANTERIOR  HORN 
ANTERIOR  ROOT 


Of  8/POL/>fr..C£LL 


AXON  Of  ANTERIOR.  HORN  CELL 


a's  TERMINATION  OF  AN.TER/OR  HORN  CELL  /N  M(/SCL£ 


FIG.  10. — Diagram  of  a  simple  reflex  arc.  Tension  changes  arising  in  the 
muscle,  affect  the  muscle  spindle  where  they  are  converted  into  nerve  ener- 
gy which  normally  passes  in  impulses  from  the  muscle  spindle  along  the 
sensory  nerve  a1,  a2,  a3,  a5  to  a6,  and  is  there  transformed  into  motor  nerve 
energy  which  passes  back  to  the  muscle  by  a7  to  the  motor  end  plate  a8  at 
which  physico-chemical  changes  are  initiated  in  the  muscle.  The  effect 
of  a  tabetic  lesion  at  o3  is  depicted 

This  junction  is  an  intimate  contact  only;  at  it,  con- 
tinuity of  nerve  substance  is  not  established ;  it  is  an  ar- 
ticulation, not  a  fusion;  the  surface  of  contact  at  the 
synapse  is  also  the  surface  of  separation.  The  physio- 
logical degeneration  of  the  severed  spinal  portion  of  the 
posterior  root  fiber  extends  to  the  termination  of  every 


24  LOCOMOTOB  ATAXIA 

branch  of  that  fiber,  but  no  further.  The  degeneration 
reaches  the  synapse  and  stops  there. 

The  cell  with  whose  processes  the  synapse  is  formed 
does  not  degenerate.  Changes,  however,  do  occur  in  it. 
These  were  formerly  thought  to  be  tabetic  but  have  now 
been  shown  to  arise  from  disuse  and  to  occur  also  in  ex- 
perimental cutting  of  the  posterior  root. 

The  axon  (a7,  Fig.  10)  of  this  anterior  horn  cell  leaver 
the  cord  by  the  anterior  nerve  root  to  terminate  (a8.  Fig. 
10)  within  the  muscle  in  which  the  muscle  spindle  lies. 

The  muscle  spindle  (Fig.  7)  is  so  formed  that  it  is 
specially  sensitive  to  the  tension  changes  which  occur 
within  a  muscle  during  stretching,  contraction  and  re- 
laxation. Acting  as  a  receptor  of  these  changes,  the 
muscle  spindle  transmutes  them  into  nerve  energy  which 
passes  in  impulses  along  the  afferent  peripheral  nerve, 
through  the  posterior  root,  and  the  posterior  horn  of  the 
spinal  cord,  to  the  synapse  with  the  anterior  horn  cell. 
A  special  afferent  path  (a,  a,1  a,2  a,3  a,5  Fig.  10)  is 
thus  constituted  for  the  impulses  evoked  by  tension 
changes  in  muscle.  These  impulses  are  not  merely  trans- 
mitted by  this  path  but  they  are  also  converted  in  it  from 
sensory  to  motor  impulses.  This  conversion  occurs  at  the 
synapse.  The  anterior  horn  cell  with  its  axon  forms 
the  efferent  path  (a,6  a,7  a,8  Fig.  10)  along  which  the 
motor  impulses  are  discharged  to  induce  changes  in 
the  muscle. 

An  afferent  sensory  path  and  an  efferent  motor  path 
linked  in  this  way  constitute  a  reflex  arc.  In  this  reflex 
arc  non-sentient  stimuli  from  the  muscle  are  converted 
into  physicochemical  action,  which  purges  the  reflex  arc 
of  them.  Such  physicochemical  action  induces  in  the 
muscle  increase,  or  diminution,  of  tone  or  irritability. 


RESULTS  OF  SYPHILITIC  LESIONS 


25 


When  a  muscle  is  stretched,  its  tone  increases ;  when  re- 
laxed, diminishes.  Upon  the  tone  of  the  muscle  its  readi- 
ness and  its  power  to  contract,  and  also  its  fatiguability, 
depend. 

This  reflex  arc,  although  ideally  composed  of  a  single 


EXTEM5OK  MUSCLE- 


FIG.  11. — Diagram  of  the  nerve  mechanism  which  correlates  the  action  of 
antagonistic  muscles.  Reflex  arcs,  a  and  6,  extensor  and  flexor  arcs  re- 
spectively, depicted,  each  with  one  alternative  path,  to  show  reciprocal 
innervation  of  anterior  horn  cells  a3  and  63. 

afferent  limb,  is  not  really  so  simply  built.  Between  the 
reflex  collateral  and  the  anterior  horn  cell  one  (a2,  Fig. 
11)  or  more  synapses  may  be  intercalated;  the  afferent 
limb,  instead  of  being  a  single  fiber,  then  consists  of  sev- 
eral fibers  (a,1  a,2  Fig.  11),  along  which  impulses  from  the 
muscle  are  relayed.  Moreover,  a  synapse  may  be  not  a 
mere  relay  station  on  an  inevitable  route,  but  a  junction 
common  to  several  routes  (a3  common  to  a2  and  b,2  Fig. 


26  LOCOMOTOR  ATAXIA 

11)  each  of  which  is  a  possible  path  for  impulses  brought 
by  the  rest.  Some  of  the  remaining  collaterals  of  the  pos- 
terior root  fiber  are  linked  ultimately  with  anterior  horn 
cells,  other  than  that  with  which  the  reflex  collateral  joins. 


1 

2  JTJTJxnJTJTJTJTJTJTJTJUTJTjruuxn^  y*i 

3  '  I 1  I- 


FIG.  12. — Diagram  to  show  a  subminimal  impulse  in  one  reflex  arc  reinforced 
by  a  subminimal  impulse  in  another  reflex  arc,  so  that  both  together  pro- 
duce a  response  which  neither  singly  can  elicit.  1,  line  of  muscle  curve;  2, 
time  marked  in  fifths  of  a  second;  3,  line  indicating  the  excitation  of  the 
one  reflex  arc;  4,  line  indicating  the  excitation  of  the  other.  A  subminimal 
stimulus  x  —  x  was  first  given  to  the  one;  no  muscular  response  followed. 
Next,  a  subminimal  stimulus  Y  —  Y  was  given  to  the  other;  no  response 
followed.  Then  x  —  x  was  applied  to  the  one  while  Y  —  Y  was  simul- 
taneously applied  to  the  other;  the  result  was  the  rhythmic  muscular 
contractions  depicted.  (Modified  slightly  from  Sherrington.) 

Therefore,  every  primary  arc  has  associated  with  it  al- 
ternative paths  for  its  impulses ;  and  every  motor  nerve 
cell  may  be  excited  by  impulses  other  than  those  proper 
to  the  particular  reflex  arc  of  which  it  forms  the  efferent 


RESULTS  OF  SYPHILITIC  LESIONS          27 

limb :  there  is  reciprocal  innervation  of  the  motor  nerve 
cells  in  the  cord;  entering  sensory  impulses  radiate 
through  the  cord. 

This  radiation  is  not  haphazard.  The  resistance  en- 
countered by  the  impulses  entering  the  cord  determines 
the  direction  in  which  they  radiate.  An  impulse  flows 
along  the  path  of  least  resistance ;  and  the  amount  of  flow 
in  alternative  paths  is  inversely  proportional  to  the  re- 
sistance these  paths  offer.  The  seat  of  the  resistance  is 
the  synapse.  In  a  moment  of  inaction  among  the  reflexes, 
the  path  of  least  resistance  to  an  entering  impulse  is  the 
primary  reflex  arc  of  the  impulse. 

A  stimulus,  unless  it  has  a  definite  minimal  intensity, 
elicits  no  reflex  response;  but  repeated  stimuli  of  an  in- 
tensity less  than  this  minimal  are  summed  in  the  arc 
until  a  response  is  produced.  Subminimal  impulses 
serve  to  lower  the  resistance  of  the  synapse,  to  facilitate 
the  passage  of  succeeding  impulses. 

After  a  motor  response,  the  reflex  arc  is  for  a  time 
markedly  less  excitable.  During  this  refractory  period, 
the  synapse  resistance  is  so  high  that  the  further  pas- 
sage of  impulses  is  blocked.  The  afferent  impulses  are 
then  diverted  from  their  usual  reflex  path  to  the  alterna- 
tive paths  which  momentarily  offer  less  resistance  than 
the  primary  reflex  arc.  These  alternative  paths  lead  to 
other  motor  nerve  cells  (to  b3  instead  of  a3  and  vice  versa, 
Fig.  11),  one  of  which  is  adequately  excited  and  gives  a 
motor  response.  In  that  reflex  arc  a  refractory  period 
ensues;  and  the  direction  of  flow  is  again  changed.  In 
addition  to  the  alternate  facilitation  and  inhibition  of 
the  passage  of  stimuli  in  the  reflex  arc,  motor  response 
is  further  correlated  by  its  constant  and  rhythmic  na- 
ture. 


28  LOCOMOTOR  ATAXIA 

When  the  extensors  of  the  knee  contract,  the  flexors 
simultaneously  relax.  According  to  McDougall,  during 
the  excitation  of  the  extensor  reflex  arc,  a  (Fig.  11),  the 
resistance  at  the  synapse,  a2,  a3,  is  lowered  to  such  an 
extent  that  impulses  traveling  in  the  flexor  arc,  b,  im- 
pulses upon  which  the  tone  of  the  flexor  depend,  finding 
their  usual  path,  b1,  b2,  b3,  offers  higher  resistance  than 
the  alternative  path,  b1,  b2,  a3,  take  the  latter  path.  The 
flexor  impulses  are  drained  from  the  flexor  arc  and  the 
tone  of  the  flexor  muscle  falls.  As  flexor  action  antago- 
nizes extensor,  the  relaxation,  or  loss  of  tone,  in  the  flexor 
muscles  permits  extensor  movement  with  a  minimum  ex- 
penditure of  energy :  inhibition  of  the  reflexes  which  sub- 
serve flexor  tone  normally  synchronizes  with  facilita- 
tion of  the  extensor  reflexes. 

In  bending  the  elbow,  when  the  arm  hangs  at  the  side, 
muscular  action  first  fixes  the  shoulder,  and  then,  while 
the  forearm  makes  with  the  upper  arm  a  smaller  and 
smaller  angle,  moves  the  upper  arm  backwards.  This 
harmonious  movement  of  the  bony  levers  of  the  skeleton 
is  called  a  synergic  movement.  Among  the  reflexes  im- 
plicated in  such  a  movement,  activity  in  one  lowers  the 
threshold  of  the  next;  and  each  succeeding  reflex  in  the 
chain  has  its  threshold  lowered  in  sequence,  so  that  the 
motor  responses  follow  one  another  in  regular  order  and 
the  associated  reflexes  constitute  a  functional  unit. 

Eesident  in  the  reflex  mechanism  of  the  spinal  cord  is 
thus  a  vast  integrating  power  of  which  the  unit  is  the 
reflex  arc  and  which  coordinates  the  muscular  activity  of 
the  individual  and  of  the  allied  segments  of  the  body. 

The  ascending  branches  of  the  sensory  fibers  of  the 
muscles,  in  their  course  through  the  posterior  columns 
of  the  cord,  are  accompanied  by  the  fibers  from  every 


RESULTS  OF  SYPHILITIC  LESIONS 


29 


receptor  of  the  tendons,  bones  and  joints.  These  segre- 
gated, ascending  branches  of  the  fibers  of  the  muscular 
apparatus  give  off  collaterals  which  form  synapses  with 
cells  of  the  columns  of  Clarke  (a1,  Fig.  13)  from  which 


FIG.  13. — To  show  relations  of  the  sensory  nerves  of  the  musculature  to  the 
cerebellum.     R  =  receptor.     For  explanation  see  text. 

arise  fibers  that  pass  in  the  tract  of  Flechsig  (Fig.  13)  to 
the  cerebellum ;  and  also  other  collaterals  which  form  syn- 
apses with  cells  of  the  column  of  Stilling  (a2,  Fig.  13) 
from  which  arise  fibers  that  pass  in  the  tract  of  Gowers, 
likewise  to  the  cerebellum.  The  ascending  branches  them- 
selves all  end  by  forming  synapses  among  the  cells  of 


30  LOCOMOTOR  ATAXIA 

the  nuclei  of  Goll  (Fig.  13)  and  of  Burdach  (Fig.  13)  in 
the  medulla,  whence  some  axons  pass,  mainly  uncrossed, 
to  the  middle  lobe  of  the  cerebellum.  Non-sentient  im- 
pulses from  the  muscular  apparatus  pass,  therefore,  by 
two  paths  to  the  cerebellum,  via  a  collateral  and  a  spino- 
cerebellar  fiber,  and  via  the  ascending  branch  and  a  med- 
ullary-cerebellar  fiber. 

In  each  internal  meatus  lie  the  bipolar  cells  of  the 
ganglion  of  Scarpa.  Their  peripheral  processes  form 
in  the  labyrinth  a  sense  organ  which  is  attuned  to  receive 
variations  in  the  pressure  of  the  otoliths  and  of  minute 
masses  of  fluid  in  the  utricle,  saccule  and  semicircular 
canals.  The  variations  are  initiated  by  change  in  the 
position  of  the  head.  The  central  processes  constitute 
an  afferent  nerve,  the  vestibular  nerve. 

The  non-sentient  of  the  impulses  from  the  labyrinth 
sense  organ  pass  along  the  vestibular  nerve,  through 
Deiters'  nucleus  (Fig.  13,  E2S2D2)  and  through  the  nu- 
cleus of  Bechterew  (Fig.  13,  K4S4B2)  to  the  anterior  horn 
cells  of  the  spinal  cord  and  to  their  homologues  among 
the  cranial  nuclei.  These  impulses  may  thus  be  distribu- 
ted to  every  reflex  arc  of  muscle  tone.  The  labyrinth  re- 
flexes adjust  the  position  of  the  eyes  and  of  the  head  to 
the  horizon.  The  attitude  of  the  head  reflexly  determines 
that  of  the  other  parts  of  the  body. 

The  vestibular  organ  of  tone  is  connected  both  directly 
(Fig.  13,  R5S5),  and  through  the  cells  of  its  subsidiary 
nuclei  (Fig.  13,  B^jVi),  most  intimately  with  the  cere- 
bellum. 

The  cerebellum  receives  impulses  from  every  receptor 
of  the  muscular  apparatus  in  the  limbs,  trunk  and  head. 
It  sends  out  impulses  to  every  motor  cell.  The  cerebellum 
is  the  central  organ  of  the  non-sentient  of  the  impulses 


RESULTS  OF  SYPHILITIC  LESIONS         31 

which  arise  in  the  muscular  apparatus;  it  is  the  center 
of  integration  not  only  of  the  segmental  reflexes  but 
of  the  reflexes  of  the  whole  musculature:  it  is  thus  the 
center  of  muscular  tone ;  of  dynamic  action ;  of  synergic 
action;  of  equilibration;  and  of  every  other  form  of 
reflexly  correlated  muscular  action.  By  virtue  of  cere- 
bellar  control  not  only  do  the  parts  of  a  limb  act  har- 
moniously in  movement  but  the  limbs  move  in  orderly 


FIG.  14. — Graphic  record  of  the  knee  jerk  to  show  its  time  relations.  (Weiler.) 
a,  records  the  movements  of  the  hammer  used  to  tap  the  patellar  tendon 
in  eliciting  the  knee  jerk;  p,  marks  the  moment  the  tap  was  administered; 
6,  traces  the  curve  of  the  leg  movements;  c,  is  the  time  record  in  1/100  seconds. 
Note  the  initial  positions  of  the  writing  points  did  not  coincide;  d,  indicates 
the  initial  position  of  the  writing  point  of  the  leg  movement,  e,  that  of  the 
writing  point  of  the  hammer  movement. 

relation  to  one  another,  and  to  the  trunk ;  *the  body  in 
motion  maintains  its  equilibrium;  and  the  entire  muscu- 
lature is  a  functional  unit. 

The  tone  of  a  muscle  depends  not  merely  on  its  local 
reflex  arc  but  also  upon  the  segmental  reflexes  allied  with 
it,  and  upon  the  vestibular  reflex :  all  are  under  the  con- 
trol of  the  cerebellum,  which  is  subject  to  cerebral  regu- 
lation. 

The  tone  of  a  stretched  muscle  is  raised,  of  a  relaxed 
muscle  is  lowered.  If  the  tone  of  the  quadriceps  be 
increased  and  that  of  the  flexors  diminished  by  bending 


32  LOCOMOTOR  ATAXIA 

the  knee,  a  tap  on  the  patellar  tendon  will  cause  a 
quadriceps  contraction  which  will  extend  the  leg.  This 
phenomenon  is  called  the  knee-jerk.  The  extent  of  the 
jerk  varies  somewhat  with  the  tap  but  mainly  with  the 
tone  of  the  extensors  and  the  relaxation  of  the  flexors. 
Formerly  we  believed  that  the  interval  between  the  tap 
and  the  jerk  was  shorter  than  the  time  necessary  for 
reflex  action  and  that  the  jerk  was  due  to  a  direct  re- 
sponse of  the  muscle.  Weiler  showed  conclusively  that  the 
interval  was  ample  (0.050  to  0.070  second)  for  reflex  ac- 
tion and  that  the  knee-jerk  was  indubitably  a  reflex  act. 

As  no  contraction  occurs  unless  the  tone  of  the  quadri- 
ceps be  adequate,  and  as  muscle  tone  is  maintained  by 
reflex  activity,  the  knee-jerk  affords  an  index  to  the 
integrity  of  the  reflex  arc  of  tone  of  the  quadriceps. 

The  briskness,  the  fatiguability  and,  in  part,  the  extent 
of  the  knee-jerk  depend  upon  the  quadriceps  tone.  The 
tone  of  the  quadriceps  is  less  in  fatigue  than  in  fresh- 
ness, after  repose  than  after  moderate  exercise. 

The  activity  of  the  cerebral  cortex  diminishes  muscu- 
lar tone.  Indeed,  hemiplegia,  supervening  on  tabes,  may 
cause  the  reappearance  of  a  lost  knee-jerk.  The  less 
attention  is  directed  to  the  knee,  the  more  does  the  tone 
of  the  muscles  there  correspond  to  the  local  conditions 
of  stretching  and  relaxation.  Measures  to  distract  the 
patient's  attention,  to  reinforce  the  knee-jerk,  are  many. 
Among  them,  those  most  used  are  engaging  him  in  con- 
versation; directing  his  gaze  upwards;  making  him,  at 
the  word  of  command,  squeeze  the  physician's  arm;  and 
inducing  him  to  hook  the  flexed  fingers  of  his  up-turned 
hand  on  those  of  his  down-turned  hand,  and  then  to 
hold  the  one  fixed  and  to  pull  strenuously  with  the  other. 

In  the  exhaustion  of  cortical  activity  due  to  the  mental 


EESULTS  OF  SYPHILITIC  LESIONS          33 

stress  which  usually  precedes  tabes,  cerebral  control  of 
reflexes  diminishes.  The  pretabetic  shows,  therefore, 
abnormally  active  tendon  reflexes.  Tendon  reflexes 
that  respond  equally  on  both  sides,  apart  from  absence, 
or  almost  absence,  may  indicate  no  structural  abnormal- 
ity. But  a  unilateral  change  in  the  extent,  the  readiness, 
the  briskness,  or  the  fatiguability  is  always  pathological. 
The  posterior  root  lesion  early  and  almost  invariably 


FIG.  15. — Demonstrating  early  hypotonia  of  the  flexor  muscles  of  the  knee 
of  a  recumbent  tabetic. 

implicates  the  afferent  fiber  of  the  reflex  arc  of  muscle 
tone.  The  particular  arc  affected  depends  upon  the  root 
diseased.  Thus  lesions  of  the  first  and  second  root 
affect  the  ankle-jerk,  the  so-called  Achilles  reflex;  of 
the  third  and  fourth  lumbar  roots,  the  patellar  reflex  or 
knee-jerk;  of  the  cervical  roots,  the  tone  reflexes  of  the 
arm  muscles ;  of  the  motor  root  of  the  fifth,  the  tone  re- 
flex of  the  jaw.  The  Achilles  reflex  is  usually  first  af- 
fected, then  the  knee-jerk.  The  arm- jerks  may  be  in- 
volved later  in  the  disease.  Usually  they  escape  alto- 
gether ;  rarely  they  are  the  first  affected.  Only  the  reflex 
on  one  side  may  at  first  be  attacked.  As  early  cases  are 


34 


LOCOMOTOB  ATAXIA 


not  often  seen,  bilateral  implication  is  most  common.  The 
various  tendons  reflexes  may  be  affected  in  all  possible 

combinations. 

When  the  afferent  of  the 
reflex  arc  of  muscle  tone  is 
attacked,  irritation  precedes 
destruction.  Exaggeration, 
therefore,  precedes  loss  of 
the  tendon  reflexes.  This 
transient  exaggeration  is 
not  often  seen.  Destruction 
quickly  follows  irritation 
and  the  jerk  becomes  of 
smaller  and  smaller  extent 
until  it  can  be  elicited  only 
by  reinforcement;  then  it 
finally  disappears. 

The  hypotonic  muscles 
tend  less  and  less  to  resist 
stretching :  they  lengthen. 
In  joints  whose  main  sup- 
port is  muscular,  abnormal 
mobility,  deformity  and 
weakness  result.  Thus,  at 
the  wrist,  hypotonia  permits 
unusual  degrees  of  flexion 
and  extension.  An  abnormal 
backward  bending  of  the 
knee  in  standing  develops 
(genu  recurvatum,  Fig.  16).  In  the  foot  the  antero- 
posterior  arch  soon  yields.  Frequently  the  tabetic  can 
assume  attitudes  as  contorted  as  those  seen  in  markedly 
rachitic  children  (Fig.  17).  The  weakening  of  joints 


FIG.  16. — Left  genu  recurvatum,  a 
case  showing  the  importance  of 
muscular  action  in  the  produc- 
tion of  this  deformity.  The  pa- 
tient had  a  shortened  right 
lower  limb  owing  to  an  old 
fracture  of  the  femur  which 
united  in  a  bad  position.  Hence, 
she  mainly  used  her  left  leg  in 
walking. 


RESULTS  OF  SYPHILITIC  LESIONS 


35 


sometimes  leads  to  dislocations,  especially  backward  dis- 
location of  the  knee  (Figs.  18  and  19).  The  elongated 
muscle  must  first  in  contracting  shorten  to  its  normal 
length  before  it  can  begin  tc  act  on  the  bony  levers  This 


FIG.  17. — Excessive  tabetic  hypotonia  permitting  a  contorted  attitude  similar 
to  that  sometimes  assumed  by  rachitic  infants. 

mechanical  disadvantage  is  minimized  by  the  speed  of 
muscular  contraction. 

The  antagonists  do  not  adequately  and  synchronously 
relax  when  the  agonists  contract.  In  the  thigh  of  a 
recumbent,  muscular  tabetic  who  is  endeavoring  to 
extend  the  flexed  leg,  one  may  sometimes  feel  the  strug- 
gle between  the  contracting  extensors  and  flexors:  to 
the  rigidity  of  both  are  added  shifting  areas  of  contrac- 
tion, according  to  the  dominance  of  which  the  leg  halts 


5  » 
II 

IH      03 


I   & 


I.    c? 
O     ti 


00      . 


36 


KESULTS  OF  SYPHILITIC  LESIONS          37 

or  jerks  onward.  The  strength  of  the  movement  is  that 
of  the  excess  of  extensor  over  flexor  action.  The  effort 
to  move  is  increased,  its  effectivity  is  diminished. 

The  anterior  horn  cell  is  the  trophic  center  of  the 
muscle.  This  cell  may  undergo  disuse  changes  owing 
to  the  destruction  of  the  reflex  collateral.  It  may  be 
directly  attacked  (S.  A.  K.  Wilson).  This  direct  attack 
is  rare  and  usually  late.  When  only  advanced  cases  of 
tabes  were  identified,  Dejerine  stated  that  twenty  per 
cent  of  tabetics  incur  muscular  atrophy.  Eulenburg,  in 
five  hundred  cases  at  all  stages,  found  this  formidable 
percentage  reduced  to  0.6.  The  usual  march  of  change 
in  electrical  excitability  is  evident  in  the  muscles  in 
these  cases. 

Besides  the  anterior  horn  cell,  its  axon  in  the  anterior 
nerve  root  or  in  the  motor  nerve  may  be  implicated. 
To  such  lesions  Dejerine  attributes  the  tabetic  "pied 
bot."  Others  have  described  a  persistent  contraction 
of  the  muscles  of  the  palm  (Figs.  20  and  21). 

But  besides  these  factors,  there  is  in  the  muscular 
weakness  of  tabes  a  factor  upon  which  stress  has  not 
been  laid,  a  factor  of  paramount  importance,  a  mental 
factor.  This  mental  factor  shows  itself  either  in  the 
readiness  with  which  fatigue  arises,  or  in  the  trifling 
muscular  power  called  forth  by  voluntary  effort  com- 
pared with  that  apparent  in  automatic  movement.  Many 
cases  have  been  described  in  which  muscular  fatigue  or 
weakness  was  an  early,  a  prominent,  but  commonly  a 
transient  symptom.  Sometimes,  in  the  tabetic,  an  ab- 
sence of  power  similar  to  that  seen  in  hysteria  is  evident 
(see  page  182).  By  suitable  therapy,  strength  may  usu- 
ally be  quickly  restored. 

When  the  syphilitic  lesion  in  the  posterior  root  com- 


38  LOCOMOTOR  ATAXIA 

pletely  severs  the  central  process  of  the  bipolar  nerve 
cell,  the  degeneration  stops  at  the  first  synapse,  the  cell 


Fig.  20 

of  w,hich  undergoes  no  consequent  change  except  that 
caused  by  disuse.    Subsequent  relay  fibers  of  the  various 


Fig.  21 

FIGS.  20  AND  21. — Syphilitic  invasion  of  anterior  horn  cells  in  a  tabetic  causing 
selective  wasting  among  the  thumb  muscles,  a  flattening  of  the  thenar  and 
hypothenar  eminences  and  a  "clawing"  mainly  of  the  ulnar  fingers. 
(Jelliffe.) 

reflexes  within  and  between  the  segments,  connecting 
and  commisural,  spinocerebellar  and  medullary-cerebel- 
lar  fibers,  do  not  degenerate.  Destruction  of  any  one  of 


RESULTS  OF  SYPHILITIC  LESIONS          39 

a  series  of  relay  fibers  is  physiologically  equivalent  to 
a  lesion  of  the  succeeding  relays,  in  so  far  as  the  function 
of  the  succeeding  relays  depends  upon  that  of  the  de- 
stroyed. Thus,  a  syphilitic  lesion  in  the  posterior  root 
causing  destruction  of  the  collaterals  which  arise  from 
the  ascending  branch  and  pass  to  the  columns  of  Clarke 
and  Stilling  (alt  a2,  Fig.  13),  is  physiologically  equivalent 
to  a  lesion  of  the  tracts  of  Flechsig  and  of  Gowers,  which 
is  equivalent  to  a  lesion  of  the  cerebellum. 

The  lesion  in  the  posterior  root  usually  severs  some 
fibers  completely  and  others  incompletely.  To  the  extent 
of  the  severance,  reciprocal  innervation  of  the  anterior 
horn  cells  is  abolished.  Fewer,  feebler  and  delayed  im- 
pulses pass  the  lesion  to  reach  the  branches  or  collaterals, 
to  attain  the  connecting  fibers;  and  the  radiation  of 
impulses  is  lessened.  Among  the  reflex  arcs  associated 
with  the  affected  fibers,  radiation  facilitates  the  passage 
of  impulses,,  With  the  lessening  of  radiation,  facilitation 
diminishes  and  its  regular  sequence  in  the  affected  arcs 
fails.  In  the  synchronous  or  successive  exciting  of  allied 
muscles  and  in  the  inhibiting  of  their  opponents,  disorder 
thence  arises.  A  loss  of  strength,  of  rhythm,  and  of 
harmony  now  becomes  evident  in  muscular  action. 

The  disintegration  of  reflex  function  varies  according 
to  the  rapidity  of  the  nerve  destruction.  The  more 
rapid  the  destruction  the  more  marked  is  its  disturbing 
effect.  But  the  first  is  not-necessarily  the  permanent 
effect.  When  a  number  of  paths  are  linked  in  a  common 
function  the  sudden  destruction  of  one  path  may  tem- 
porarily disorganize  the  whole  function.  But  the  re- 
maining paths  may  quickly  adapt  themselves  to  the  loss 
of  their  fellow  and  to  a  considerable  degree  compensate 
for  it. 


40 


LOCOMOTOR  ATAXIA 


The  disturbance  of  reflex  integration  produced  by 
lesions  differing  only  in  site,  is  most  severe  when  the 
lesion  is  in  the  cerebellum;  more  grave  when  in  the 
vestibular  organ  than  when  in  the  spinal  cord;  and 
when  in  the  spinal  cord,  is  less  and  less  important  the 
further  the  affected  roots  are  from  the  head  segment. 

Every  movement  is  a  part  of  a  greater  movement, 

Anus  4  vagina. 


cords. 


FIG.  22. — Chimpanzee's  brain.     To  show  motor  and  sensory  areas  of  brain 
cortex.     (After  Sherrington-Grunbaum.) 

which  in  turn  is  a  section  of  the  movement  of  the  muscu- 
lature as  a  whole.  The  demolition  of  any  part  of  this 
functional  unit  affects  the  whole  to  a  degree  which  de- 
pends upon  the  site,  the  extent  and  the  rapidity  of 
development  of  the  destruction  and  upon  the  power  of 
compensation  which  is  inherent  to  the  coordinating 
mechanism  that  remains  structurally  unaltered. 

The  amount  of  reflex  disturbance  is  difficult  to  deter- 


FIG.  23. — Diagram  showing  the  course,  origin  and  termination  of  the  fibers 
of  the  principal  tracts  of  the  white  matter  of  the  spinal  cord.   • 

"Descending"  tracts:  la,  a  fiber  of  the  crossed  pyramid  or  corticospinal 
tract;  Ib,  an  uncrossed  fiber  of  the  pyramid  or  corticospinal  tract  passing 
to  the  lateral  column  of  the  same  side;  2,  a  fiber  of  the  ventral  pyramid  or 
corticospinal  tract;  3,  a  fiber  of  the  ventrolateral  descending  or  ponto- 
spinal  tract;  4,  a  fiber  of  the  rubrospinal  tract;  5,  a  fiber  of  the  comma  tract. 
"Ascending"  tracts:  6,  a  fiber  of  the  dorsomesial  spinobulbar  tract;  7, 
fibers  of  the  dorsolateral  spinobulbar  tract;  9,  one  belonging  to  the  dorsal 
spinocerebellar;  10,  a  fiber  of  the  ventral  spinocerebellar  tract.  (Quain's 
"Anatomy,"  published  by  Longmans,  Green  and  Co.) 


41 


42  LOCOMOTOR  ATAXIA 

mine  except  in  such  simple  reflexes  as  the  knee-jerk, 
for  movement  is  voluntary,  not  reflex.  In  adult  life, 
we  desire  a  posture  and  its  attainment  more  or  less 
automatically  follows.  The  desire  excites  a  postural 
image.  The  association  between  a  postural  image  and 
its  reproduction  is  fixed  by  the  mordant  influence  of 
years. 

The  motor  reproduction  of  the  postural  image  is 
elicited  through  the  Eolandic  area  of  the  cerebral  cortex.. 
The  pyramidal  tract  fiber  that  passes  from  the  cell  of 
the  Rolandic  area,  through  the  corona  radiata,  internal 
capsule,  pons  and  medulla,  ends  in  the  motor  cell  of  the 
anterior  horn  of  the  spinal  cord  or  in  its  homologue 
among  the  basal  nuclei.  The  cortical  activity  is  dis- 
charged through  the  axons  of  the  anterior  horn  cells  to 
evoke  muscular  movements. 

The  movements  excited  at  the  Rolandic  area  by  elec- 
trical stimulation  are  divided  by  Sherrington  into  three 
groups : 

' '  In  one  group,  movement  evoked  from  the  cortex  of  one  hemi- 
sphere seems  a  fraction  of  the  natural  movement,  the  natural 
movement  requiring  in  its  completeness  the  corroboration  of  the 
symmetrical  area  of  the  cortex  of  the  opposite  hemisphere.  In 
a  second  group,  instanced  by  conjugate  lateral  deviation  of  the 
eye-balls  toward  the  opposite  side,  it  is  equally  obvious  that  the 
reactions  of  symmetrical  areas  of  the  right  and  left  cortices  are 
related  to  one  another  as  antagonistic  reactions.  In  a  third  group 
of  cases,  the  reactions  of  symmetrical  cortical  areas,  right  and 
left,  seem  neutral  to  one  another.  Thus,  with  the  area  which 
yields  movement  of  the  thumb,  that  reaction  seems  neither  to  re- 
inforce nor  to  interfere  with  the  similar  reaction  evoked  from 
the  identical  area  of  the  opposite  hemisphere." 

Thus,  cortical  motor  cells,  just  as  the  motor  cells  of 
the  spinal  cord,  show  reciprocal  innervation  and  the 


RESULTS  OF  SYPHILITIC  LESIONS 


43 


phenomena  which  result  from  it.  The  motor  reactions 
elicited  through  the  reflex  mechanism  can  be  duplicated 
by  stimulation  of  the  cerebral  motor  cortex.  Cerebral 
and  spinal  activities  are  conveyed  to  the  muscles  along 
a  common  path,  the  axon  of  the  anterior  horn  cell,  the 
peripheral  motor 
nerve.  Cortical  ex- 
citation of  muscles 
may,  therefore,  rein- 
force reflex  excita- 
tion. Hence  cortical 
action  may  compen- 
sate in  some  degree 
for  loss  of  reflex  ac- 
tion, may  mask  dur- 
ing movement  reflex 
defects. 

Before  reflex  dis- 
integration is  visible 
to  the  naked  eye  it 
may  be  detected  in 
graphic  records  of 
movements,  e  s  p  e  - 
cially  of  the  exag- 
g  e  r  a  t  e  d  defensive 
withdrawal  of  the 
lower  limb  which, 
after  delay  perhaps,  follows  scratching  of  the  sole  of 
the  tabetic  foot. 

In  such  a  graphic  record  may  be  evident  that  the 
antagonists  do  not  adequately  relax  when  the  agonists 
contract.  Muscles  acting  similarly  on  the  same  bony 
lever  do  not  contract  synchronously  and  the  wonted  con- 


FIG.  24. — The  three  stages  In  the  normal 
grasp.     (Graham  Brown.) 


44 


LOCOMOTOR  ATAXIA 


sonance  of  muscles,  acting  simultaneously  on  different 
levers  in  a  complex  movement,  is  lacking.  The  absence 
of  relaxation  in  the  antagonists  may  even  be  palpable. 
The  lack  of  consonance  (asynergia)  may  be  obvious  in 
an  affected  upper  limb  on  closing  the  fist :  the  extension 
of  the  hand  on  the  wrist  which  normally  occurs  syn- 

chronouslywith 
the  contraction 
of  the  flexors  of 
the  fingers,  dis- 
appears ;  the 
closed  fist  is  no 
longer  bent 
back  on  the 
forearm ;  f  i  s  t 
and  forearm 
are  either  in 
the  same 
straight  line  or  the  fist  is  bent  forward  (Fig.  25). 

In  tabes  cerebral  action  may  mask  reflex  defects.  Re- 
flex defects  are  not  revealed  during  voluntary  movement 
until  the  cerebral  control  fails :  the  amount  revealed 
depends  on  the  degree  of  the  failure.  The  tabetic  moves 
by  his  brain  to  the  extent  necessitated  by  the  reflex 
disintegration.  Defective  voluntary  movements,  ataxic 
movements,  are  no  index  to  the  degree  of  the  reflex 
disturbance. 


FIG.  25. — The  tabetic  grasp  showing  asynergia: 
normally  in  grasping,  the  hand  makes  with  the 
forearm  an  obtuse  angle;  here  the  hand  and  fore- 
arm are  in  the  same  straight  line.  (Graham 
Brown.) 


CHAPTER  III 

RESULTS  OF  THE  SYPHILITIC  LESIONS 

2.  DISTURBANCE  OF  SENSORY  FUNCTION 

Course  of  the  sensory  impulses  from  the  periphery  to  consciousness. 
Specific  nature  of  the  impulses  conducted  by  sensory  fibers.  Sen- 
sory images.  Factors  which  determine  the  fate  of  the  sensory 
images.  The  peripheral  impulse  and  the  mental  reaction  to  it. 
Measurement  of  stimuli.  Sensory  thresholds.  Their  variability. 
Complex  content  of  the  sensation  which  arises  from  a  simple 
stimulus.  Sensory  results  of  a  complete  and  of  an  incomplete 
lesion  of  the  posterior  root.  Selective  invasion  of  the  root  fibers 
conducting  pain.  Touch  loss.  Temperature  loss.  Vibration  loss. 
The  postural  sense.  Paths  of  sensory  fibers  from  the  muscular 
apparatus  and  from  the  postural  sense  organ  of  the  head.  Loss  of 
the  sense  of  the  body's  posture.  Measurement  of  the  loss  of  postu- 
ral sense.  Effect  of  blindness  and  of  training  on  postural  sense  in 
the  non-tabetic  and  in  the  tabetic.  Variability  of  postural  sense 
loss.  Postural  sense  loss  inaccurate  index  of  the  severity  of  the 
tabetic  lesions. 

THE  peripheral  processes  of  the  spinal  ganglion  cells 
terminate  in  sensory  receptors,  some  of  which  respond 
only  to  touch,  others  to  pain,  others  again  to  tempera- 
ture, still  others  to  pressure.  Of  the  central  processes 
some,  therefore,  conduct  only  tactile  impulses,  others 
pain  impulses,  others  again  temperature  impulses,  and 
still  others  tension  impulses.  The  sensory  impulses  aris- 
ing in  the  peripheral  receptors  pass  by  the  posterior  root 
fibers  to  their  first  cell  station  in  the  nuclei  of  Goll  and  of 
Burdach.  Then  the  sentient  of  these  impulses  are 
conveyed  by  a  second  relay  of  fibers  to  the  ventrolateral 
region  of  the  opposite  optic  thalamus,  their  second  cell 

45 


-F.  cortica- 
thalain. 


Intercalated 
cell 


Dorsal  column 

sensory  paths 


XN.  Crossed  secondary 
^  „"  ~  sensory  paths 


FIG.  26. — To  represent  diagrammatically  the  anatomical  arrangement  of  the 
paths  and  centers  concerned  in  sensation.  Two  distinct  paths  exist  in  the 
spinal  cord;  a  crossed  secondary  path  in  the  ventrolateral  column  which 
conveys  impressions  of  pain,  temperature  and  touch,  and  a  second  uncrossed 
path  in  the  dorsal  column  which  also  carries  touch,  and  in  which  run  im- 
pulses that  underlie  the  sense  of  position,  the  appreciation  of  movement, 
the  discrimination  of  two  points,  and  the  recognition  of  vibration,  size, 
shape,  form,  weight  and  consistence.  This  second  path  decussates  in  the 
lower  part  of  the  medulla  oblongata,  but  runs  separate  from  the  first  path 
at  least  as  high  as  the  pons.  All  these  secondary  sensory  fibers,  now 
crossed,  terminate  in  the  ventrolateral  region  of  the  optic  thalamus.  The 
impressions  they  carry  are  regrouped  here  and,  through  intercalated 
neurones,  are  distributed  along  two  distinct  paths;  the  one  carries  impres- 
sions to  the  cerebral  cortex,  the  other,  we  assume,  towards  the  more  mesial 
parts  of  the  optic  thalamus.  The  corticothalamic  fibers,  which  terminate 
in  the  lateral  nucleus  of  the  optic  thalamus,  are  also  shown.  (Head  and 
Holmes.) 

46 


RESULTS  OF  SYPHILITIC  LESIONS         47 

station.  A  third  relay  of  fibers  conveys  them  to  the 
cerebral  cortex  where  they  excite  sensory  images.  The 
nature  of  the  exciting  impulses  these  fibers  conduct  deter- 
mines the  nature  of  the  images  excited  in  the  cortex. 

The  fate  of  the  newly  excited  sensory  images  depends 
chiefly  upon  their  power  to  command  attention.     That 

A 


B 


FIG.  27. — Von  Frey's  Hairs  (Barker)  affixed  with  sealing  wax  to  wooden 
handles;  A,  the  hair  applied  to  the  skin  surface,  F  (F  should  show  dimpling 
as  in  B) .  With  every  hair  a  maximum  pressure  may  be  applied.  Beyond 
that  maximum  the  hair  bends.  B  shows  the  effect  of  attempting  to  apply 
a  pressure  greater  than  the  force  with  which  the  hair  can  resist  bending. 

power  increases  with  their  profusion  and  with  their 
intensity.  Whether  a  sensory  demand  for  attention  be 
or  be  not  successful,  depends  not  only  upon  the  power  of 
that  demand  but  also  upon  the  power  of  other  and  simul- 
taneous demands  and  upon  the  available  store  of  atten- 
tion. 

The  amount  of  attention  which  the  newly  excited 
images  gain  is  devoted  to  associating  them  with  analo- 
gous images  of  past  experiences  that  are  stored  in 
memory.  By  the  gained  ampunt  of  attention,  the  asso- 
ciation of  the  present  images  with  the  memory  images  of 


48 


LOCOMOTOR  ATAXIA 


the  same  order  is  facilitated  and  the  association  of  all 
sensory  images  alien  to  that  order  is  inhibited.  If  the 
facilitation  be  adequate,  the  sensory  images  excited  by 
the  peripheral  stimuli  evoke  a  sensation,  the  stimuli  are 
perceived.  If  the  facilitation  be  inadequate,  no  sensa- 
tion arises,  the  newly  excited  images  are  unconsciously 
suppressed,  the  stimuli  are  ignored. 

By  instruments  which  apply  measured  touch    (von 
Frey's  hairs),  pain  (algesimeter),  pressure  touch  (aesr 


Number  by 
which  the 

Pressure  in 

Measured  radii 

Total  area 

Radius  of  a 
circle  of  the 

Pressure  per  unit 

Tension 

hair  is 
known 

grammes 

M 

in  mm. 

same  area  in  p 

area 

8 

0-04 

30     x     54 

0-005 

40 

8  grin.  /mm. 

1  grm./mm. 

12 

0-1 

47-5  x     57-5 

0-0085 

52 

12  gnu.  /mm. 

2  grm./mm. 

14 

0-21 

85     x     90 

0-015 

70 

14  grm./mm. 

3  grm./mm. 

21 

0-23 

40     x    80 

0-011 

58 

21  grm./mm. 

4  grm./mm. 

21 

0-36 

60     x     90 

0-017 

73-5 

21  grm./mm 

5  grm./mm. 

23 

0-88 

100     x  120 

0-0377 

110 

23  grm./mm 

8  grm./mm. 

35 

1-4 

100     x  130 

0-041 

114 

35  grm./mm 

12  grm./mm. 

40 

1-8 

115     x  125 

OO45 

120 

40  grm./mm 

15  grm./mm. 

70 

3 

115     x  115 

0042 

115 

70  grm./mm 

26  grm./mm. 

90 

3-6 

100     x  130 

0-011 

114 

90  grm./mm 

32  grm./mm. 

100 

3-5 

80     x  140 

0-035 

110 

100  grjn./mm 

32  grm./mm. 

110 

4-8 

105     x  130 

0-044 

120 

110  grm./mm 

40  grm./mm. 

FIG.  28. — Table  of  von  Frey's  hairs.     (Head  and  Holmes.) 

thesiometer),  pressure  pain  (algometer),  or  other 
stimuli,  we  can  ascertain  the  minimal  stimulus  of  a  given 
order,  which  at  a  given  site,  can  evoke  a  sensation.  This 
minimal  value  marks  the  threshold  below  which  stimuli 
are  not,  as  a  rule,  perceived. 

When,  say,  touch  is  tested  in  an  attentive  person,  if 
subliminal  stimuli  be  first  applied,  delusions  of  touch  may 
arise  and  may  persist,  until,  with  an  adequate  stimulus, 
an  unimpeachable  sensation  of  touch  is  evoked  which 
affords  a  criterion  for  further  judgment.  When  stimuli 
are  applied  in  succession  from  a  normal  to  a  contiguous 
area  of  sensory  loss,  the  extent  of  the  area  of  sensory 
loss  is  smaller  than  when  the  stimuli  march  from  the 
insensitive  to  the  normal  area.  A  positive  response 


RESULTS  OF  SYPHILITIC  LESIONS 


49 


B 


may  thus  be  given  to  an  imperceptible  stimulus  and  a 
negative  response  to  a  perceptible  stimulus.  The  re- 
sponse elicited  is  the  resultant  of  two  factors,  the 
peripheral  stimulus  and  the  mental  reaction. 

No  sensory  threshold  is  ^ 

constant:  it  varies  as  the 
attention  ebbs  and  flows. 
It  is  higher  in  fatigue 
than  in  freshness,  in  de- 
pression than  in  cheerful- 
ness, in  apathy  than  in  in- 
terest. The  simpler  the 
perception,  the  less  evi- 
dent is  this  oscillation ;  the 
more  complex,  the  more 
evident.  Hence,  the  sim- 
plest sensations  evoked 
by  peripheral  stimuli 
serve  best  as  a  guide  to 
the  integrity  of  the  con- 
ducting paths.  Complex 
sensations,  such  as  are  in- 
volved in  weight  appre- 
ciations, are  more  suited 
for  mental  tests  than  for 
sensory. 

Between  successive  sen- 
sory perceptions  there  are 


-8 


Uo-- 


FIG.  29.  —  Algesimeter.  (Head  and 
Holmes.)  By  moving  the  regulator, 
E,  the  tension  of  the  spring  can  be 
increased  or  diminished  to  an  extent 
measurable  on  the  scale,  a — b.  The 
penetrating  force  of  the  needle  point, 
C,  necessary  to  elicit  pain,  can  thus 
be  approximately  ascertained  in 
terms  of  this  arbitrary  graduation. 


three  measurable  variables:  the  rate,  the  direction,  and 
the  extent  of  the  change.  As  a  rule,  only  the  last  is 
clinically  used.  The  average  minimal  perceptible  stim- 
ulus in  all  mental  states  is  taken  as  the  sensory  thres- 
hold. The  extent  of  the  sensory  loss  is  that  revealed 


50 


LOCOMOTOR  ATAXIA 


when  testing  only  from  the  normal  to  the  anaesthetic 
area.  The  distribution  of  the  sensory  loss  indicates  the 
locality  and  extent  of  the  lesions. 

Touch  stimuli  are  supposed  to  differ  from  pressure 
stimuli  in  that  the  latter  deform  the  skin  surface.  Every 
touch  deforms  the  skin.  Von  Frey  adopted  arbitrary 


WEIGHTS 


\--STEEL  PLUNGER. 
...WEIGHT  SHELF 


I 


c 


....3 


-CORK  TIP 
PRESSURE  SURFACE. 

FIG.  30. — Pressure  esthesiometer  (Holmes)  for  testing  pressure  touch.  By 
means  of  the  gram  weights,  threaded  upon  the  steel  plunger  B,  resting 
on  the  weight  shelf  C,  the  pressure  on  the  unit  area  of  the  cork  tip  which 
is  applied  to  the  skin  can  be  varied. 

standards  to  define  touch  from  pressure.  Pressure  be- 
yond a  certain  power  elicits  pain.  Pain  induced  by 
pinprick  implies  a  touch.  A  temperature  stimulus  has 
usually  a  touch  and,  if  of  sufficiently  high  or  low  degree, 
a  pain  element  also.  The  sensation  contains  not  only  the 
character  of  all  the  specific  impulses  which  evoke  it,  but 


RESULTS  OF  SYPHILITIC  LESIONS 


51 


-—INDICATOR 


-GRADUATED 
PWNGEK 


also  that  of  the  site  stimulated.    Both  the  nature  and 
the  localization  of  the  stimuli  are  perceived. 

If  the  syphilitic  lesion 
completely  severs  the  pos- 
terior root,  all  the  im- 
pulses which  the  affected 
fibers  convey  from  their 
sensory  receptors  are  en- 
tirely blocked.  -No  im- 
pulses pass  the  lesion;  no 
impulses  reach  the  corre- 
sponding cells  of  the 
synapses  at  the  nuclei  of 
Goll  and  of  Burdach;  no 
impulses  pass  thence  to 
the  cortex;  no  images  are 
excited;  no  sensations  are 
evoked,  however  much  the 
sensory  receptors  of  the 
destroyed  root  be  stimu- 
lated. A  lesion  in  the  first 
of  these  three  relays  of 
fibers  which  are  linked  in 
a  common  function  is  thus 
physiologically  equivalent 
to  a  lesion  of  all  three 
relays. 

The  lesion  in  the  pos- 
terior root,  if  incomplete, 
seldom  affects  the  various 
sensory  groups  synchron- 
ously or  equally ;  thus,  the  pain  loss  is,  as  a  rule,  the  first, 
the  most  extensive  and  the  most  severe.  The  syphilitic 


._J>R£SSURE 
SURFACE. 

FIG.  31. — Modified  Cattell  algometer 
for  measuring  pressure  pain.  The 
pressure  surface  is  applied  to  the 
supported  investigated  area  and 
pressure  is  exerted  upon  the 
knobbed  end.  As  the  pressure  in- 
creases, the  plunger,  P,  is  pushed 
up  into  the  case  while  the  indicator 
is  forced  down  the  scale.  After 
the  pressure  has  been  removed  from 
a  part  in  which  a  pressure  of  3J^ 
kilos  per  unit  area  produced  pain, 
the  position  of  the  indicator  would 
be  that  shown  in  B.  The  algometer 
may  be  obtained  graduated  in  kilos 
or  in  pounds. 


52  LOCOMOTOR  ATAXIA 

lesion  in  the  posterior  root  tends  to  affect  the  root  fibers 
in  functional  groups  and  within  these  groups  to  implicate 
the  fibers  unequally.  Some  fibers  may  be  completely 
severed,  some  may  escape,  some  may  be  partially  de- 
stroyed. As  a  rule,  the  axis  cylinder  persists,  but  it 
may  shrink  and  undergo  microscopic  changes  which  we 
little  understand.  The  myelin  sheath  degenerates.  It  is 
said  both  to  isolate  the  axis  cylinder,  so  that  the  impulses 
conveyed  may  be  confined  to  their  course ;  and  to  increase 
the  conductivity  of  the  nerve.  But  nerve  impulses  en- 
counter resistance  mainly  at  the  synapse.  The  resistance 
at  the  synapse  is  high  in  conditions  of  defective  nutrition 
of  the  neurons.  Resistance  is  notably  raised  at  the 
synapse  of  a  nerve  process  partially  severed  by  a  syph- 
ilitic lesion  in  the  posterior  root  from  its  food  supply, 
the  ganglion  cell.  The  more  complete  the  severance,  the 
higher  is  the  resistance,  the  higher  the  sensory  threshold. 

The  passage  of  impulses  is  swifter  along  the  nerve 
fiber  than  through  the  synapse.  The  higher  the  resist- 
ance at  the  synapse,  the  more  is  the  delay  in  passing 
there.  Delayed  perception,  which  is  frequently  seen  in 
tabetics,  is  a  sign  of  an  incomplete  lesion.  As  a 
phenomenon  of  an  incomplete  lesion  we  must  add  to  a 
raised  threshold  and  delayed  perception  a  sensation  of 
imperfect  content.  Thus,  touch  in  tabes  may  be  per- 
ceived, and  yet  be  imperfectly  localized;  pinprick  may 
be  felt  as  a  touch  without  any  pain  element;  pressures 
almost  injurious  to  the  tissues  may  induce  no  pain;  a 
burn  may  provoke  merely  a  sensation  of  warmth. 

In  tabetics,  areas  of  complete  insensitivity,  especially 
to  pain,  or  of  diminished,  delayed  and  imperfect  sensi- 
tivity occur.  Such  areas  are  encountered  usually  first 
on  the  lower  limbs ;  next,  most  frequently,  on  the  thorax ; 


RESULTS  OF  SYPHILITIC  LESIONS          53 

then,  on  the  ulnar  side  of  the  arms ;  then  on  the  remainder 
of  the  trunk;  and  last  on  the  head  and  neck  and  face. 
In  the  lower  limbs  the  area  of  the  fifth  lumbar  and  first 
sacral  roots  is  usually  first  affected;  on  the  thorax,  the 
breast.  But  the  sensory  loss  may  exceptionally  begin 
at  other  sites  and  may  predominate  there. 

Among  the  fibers  conducting  impulses  of  the  same 
order,  the  long  are  usually  first  and  most  severely  im- 
plicated. Thus,  the  sensory  loss,  as  a  rule,  is  greater 
over  the  feet  and  hands  than  over  the  less  distal  parts 
of  limbs,  and  greater  over  the  front  than  over  the  back 
of  the  thorax. 

The  loss  of  tactile  sensibility  usually  has  an  evident 
root  distribution.  Associated  with  this  loss  are  trouble- 
some paraesthesias,  sensations  of  insects  crawling  upon 
the  skin,  of  tingling  and  of  numbness.  The  patient  may 
feel  as  if  he  walked  on  rubber  or  on  felt  or  on  cotton 
wool.  Similar  sensations  are  experienced  in  walking 
after  cocainization  of  the  skin  of  the  soles  of  the  feet. 

Preceding  tactile  loss,  loss  of  sensibility  to  pinprick 
invariably  occurs.  Sites  which  show  at  first  merely  a 
blunting  of  pain  sensibility  may  speedily  become  quite 
analgesic.  There  may  be  delay  in  perceiving  pain 
stimuli,  then  a  sudden  exaggerated  response,  followed 
by  unwonted  persistence  of  the  painful  impression.  The 
loss  -may  be  total;  the  strongest  stimulus  of  the  algesim- 
eter  may  be  perceived  not  at  all,  or  merely  as  a  touch. 

From  the  temperature  sense  not  only  the  pain  and  the 
touch  but  also  the  essential  thermal  element  may  dis- 
appear. On  skin  areas  where  a  change  of  three  to  five 
degrees  may  normally  be  appreciated,  twenty  or  thirty 
degrees  of  difference  may  pass  undetected.  Usually  the 
tabetic  can  tell  a  change  has  occurred  before  he  can 


54 


LOCOMOTOR  ATAXIA 


detect  whether  it  is  hotter  or  colder.  Associated  with 
temperature  loss,  sensations  of  burning  or  of  sudden 
trickling  of  cold  or  of  hot  water  may  arise  in  the  limbs. 


FIG.  32. — Muscle  spindle.     (Dogiel,  Graham  Brown.) 

Egger  and  Dejerine  have  emphasized  the  loss  of  vi- 
bration sense  in  tabes.    This  loss  affects  simultaneously 


FIG.  33. — Tendon  organ.     (Dogiel,  Graham  Brown.) 

the  bones,  muscles  and  subcutaneous  tissues,  and  may  be 
coextensive  with  the  loss  of  pain. 

The  sensory  receptors  in  muscles,  tendons,  ligaments 


EESULTS  OF  SYPHILITIC  LESIONS 


55 


and  cartilage  are  attuned  to  respond  to  changes  in  the 
muscular  apparatus.  Sentient  impulses  from  these  re- 
ceptors pass  along  the  common  afferent  nerve  through 
the  posterior  roots  and  thence  by  the  sensory  relays  to 
the  cerebral  cortex.  The  sensory  receptors  in  the  laby- 
rinth of  the  ear  (page  30)  are  attuned  to  respond  to 
change  of  the  planes  of 
the  head.  Sentient  im- 
pulses travel  from  these 
receptors  by  the  vestibu- 
lar  nerve  to  the  vestibular 
nucleus,  thence  to  the  op- 
tic thalamus  and  finally  to 
the  cortex. 

Sentient  impulses  from 
the'  muscular  apparatus 
and  from  the  labyrinthine 
organ  are  constantly  ex- 
citing in  the  cerebral  cor- 
tex kaleidoscopic  postural 
images  of  the  whole  body, 
always  changing,  yet  al- 
ways related.  Of  the  ma-  FIG.  34.— Ruffini's  corpuscle,  from 

jority  of  these  images  we 
are  unconscious.  Were  we 
constantly  aware  of  our  posture,  we  could  not  think 
unless  we  were  absolutely  at  rest.  Even  when  we 
are  concentrating  attention  upon  postural  images,  we 
are  conscious  neither  of  all  the  postural  images  nor  of 
all  the  changes  in  them.  *  Only  the  most  persistent,  the 
final,  or  the  intrinsically  dominant  of  the  postural  images, 
or  the  resultant  from  a  series  of  successively  evoked 
images,  or  from  a  group  of  such  series,  may  reach  con- 


ligament  of  knee.    (Sfameni,  Gra- 
ham Brown.) 


56  LOCOMOTOR  ATAXIA 

sciousness.  We  are  usually  conscious,  not  of  the  postures 
of  the  various  parts  of  the  body,  but  only  of  their  com- 
bined effect,  of  our  relation  to  our  environment.  In  this 
combined  effect,  the  importance  of  the  several  parts 
varies  according  to  the  posture ;  but  except  in  the  recum- 
bent posture  the  attitude  of  the  head  dominates  our 
conception  of  the  body's  posture. 

The  lesion  of  the  posterior  root  may  partially  or  com- 
pletely interrupt  the  sensory  impulses  underlying  ap- 
preciation of  position  in  any  section  of  the  body.  Lesions 
in  the  head  segment,  labyrinthine  affections,  are  more 
disturbing  than  lesions  elsewhere  and  lesions  of  the  trunk 
than  lesions  of  the  limbs,  and  lesions  of  the  lower  than 
those  of  the  upper  limbs. 

Loss  of  the  sense  of  the  body's  posture  has  not  been 
measured.  The  gross  content  of  this  relation  is  some- 
times so  distorted  that  tabetics,  when  recumbent  and  at 
rest,  feel  as  if  they  were  rotating ;  and  when  erect,  as  if 
they  were  reeling  or  falling. 

Loss  of  the  sense  of  posture  in  a  section  of  the  body, 
a  limb  or  a  part  of  a  limb,  has  been  estimated  by  dupli- 
cating with  its  fellow,  reproducing  on  a  mannikin,  or 
describing,  the  position  and  attitude  of  the  investigated 
section.  An  existing  posture  is  changed  to  a  new  one 
through  a  series  of  intermediate  postures.  Most  clini- 
cians use  the  appreciation  of  this  change  as  an  index  to 
the  power  of  appreciating  posture,  an  index  to  the  so- 
called  postural  sense. 

Goldscheider  showed  that  with  a  constant  rate  a  certain 
minimal  extent  of  passive  movement  is  normally  needful 
before  a  postural  change  can  be  detected.  This  extent 
varies  in  different  joints ;  the  threshold  for  large  joints 
is  lower  than  for  small.  The  threshold  is  not  of  constant 


RESULTS  OF  SYPHILITIC  LESIONS          57 

value.  In  testing  a  finger  joint,  movements  through  an 
arc  of  5°,  of  6°,  and  of  4°,  may  be  respectively  necessary 
to  elicit  a  response  in  three  successive  trials.  The  thresh- 


FIG.  35. — Goldscheider's  instrument  (model  used  by  Head  and  Holmes)  for 
measuring  joint  movements.  By  means  of  the  bands,  B,  the  metal  plate,  A, 
is  immovably  attached  to  the  limb,  proximal  to  the  moving  joint,  and  in 
the  plane  of  the  movement:  Into  the  slot,  D,  the  scale  is  inserted.  The 
joints  at  D  and  E  permit  the  scale  to  be  rotated  into  any  plane  without 
detaching  the  plate  A.1 

old  varies  with  the  attention,  but  its  average  value, 
5°,  is  practically  constant  in  the  same  joint  in  the  same 
individual.  Simultaneously  with  the  appreciation  of 

1  These  instruments  for  measuring  sensation  can  be  obtained  from 
the  Dressier-Beard  Mfg.  Co.,  New  York  City. 


58  LOCOMOTOR  ATAXIA 

movement  comes  ordinarily  the  appreciation  of  direction ; 
both  normally  have  the  same  threshold. 

The  syphilitic  lesion  of  the  posterior  roots,  if  com- 
pletely severing  the  fibers  conveying  the  impulses  under- 
lying postural  sense,  entirely  abolishes  perception  of 
posture  in  a  joint.  If  the  severance  be  incomplete,  the 
greater  the  destruction  is,  the  feebler,  more  delayed  and 
more  sparse  are  the  impulses  which  reach  the  cortex  to 
excite  postural  images;  and  the  higher  is  the  threshold. 
for  perception  of  movement.  Movement,  if  appreciable 
at  all,  must  be  of  abnormally  great  extent  before  it 
can  be  detected :  then  its  direction  still  remains  unknown. 
The  movement  may  need  to  be  increased  fifty  per  cent 
or  more  before  the  direction  is  discerned.  The  threshold 
of  direction  is  higher  than  the  threshold  of  movement. 

The  lower  limbs  are  more  often  affected  than  the 
upper ;  the  head  rarely  escapes.  There  may  be  complete 
loss  of  postural  sense  in  the  toes.  The  ankle  is  more 
affected  than  the  knee,  the  hip  less  than  either.  Similarly 
the  shoulder  is  less  and  the  finger  more  affected  than 
the  elbow  or  wrist.  Loss  in  the  large  joints  never  rivals 
that  in  the  small. 

After  a  sensation  of  a  given  order  has  been  evoked 
by  a  perceptible  stimulus,  before  a  change  can  be  per- 
ceived, the  intensity  of  a  superadded  stimulus  must  bear 
a  certain  ratio  to  that  of  the  existing  stimulus.  The 
amount  of  change  necessary  for  detection  varies  with 
the  sensory  order:  a  change  of  one  eightieth  to  one 
hundredth  in  the  intensity  of  visual  stimuli  can  be  de- 
tected: of  about  one-seventh  in  auditory  stimuli.  Al- 
though such  average  values  may  be  determined,  the 
threshold  of  perception  of  change  presents  individual 
variations  of  considerable  extent.  Musicians  may  be 


RESULTS  OF  SYPHILITIC  LESIONS          59 

able  to  detect  tone  differences  which  are  imperceptible 
to  the  untutored  ear.  Slinger  and  Horsley,  reporting 
their  investigations  of  the  muscular  (postural)  sense 
among  the  students  of  a  college  for  the  blind,  state: — 

"  ...  if  the  information  gained  by  sight  is  permanently 
blotted  out,  the  muscular  sense  under  necessity  can  by  educa- 
tion be  brought  to  a  point  at  least  one-fourth  better  than  that 
learnt  by  the  normal  seeing  individual.  In  confirmation  of  this 
conclusion,  the  plate  test  showed  in  a  very  striking  manner  that 
the  pupils  who  were  completing  the  technical  training  of  the 
college  were  notably  superior  to  those  who  were  just  entering  on 
their  special  education." 

Blind  tabetics  possess  a  remarkable  freedom  from 
postural  sense  loss.  This  freedom  is  in  part  due  to  the 
localization  of  the  lesions,  but  in  a  tabetic  who  had 
lately  become  blind  I  was  able  to  measure  the  subsequent 
improvement  in  the  postural  sense.  Forster,  comparing 
a  group  of  blind  with  a  group  of  seeing  tabetics,  found 
loss  of  touch,  a  perception  demanding  little  discrimina- 
tion, approximately  equal  in  both  groups :  whereas  pos- 
tural sense  appreciation  was  faulty  in  eight  of  the  seeing 
but  in  only  four  of  the  blind. 

Balancers  and  jugglers  and  others  who  specialize  in 
movement  have  more  acute  discrimination  of  posture 
than  ordinary  individuals.  By  the  courtesy  of  Dr. 
Wachsmann,  Director  of  the  Montefiore  Home,  I  demon- 
strated to  the  students  of  the  International  Extension 
Course  at  Fordham  University  in  1912,  a  patient  who 
was  a  professional  skater,  who  for  over  seven  years  had 
had  nearly  every  tabetic  sign,  but  only  insignificant  pos- 
tural loss.  I  have  treated  three  sailors,  one  officer  and 
two  common  seamen,  who  were  long  tabetic,  and  who 


60  LOCOMOTOR  ATAXIA 

showed  pain,  tactile  and  pressure  loss,  but  only  slight 
postural  sense  loss. 

By  psychotherapy,  the  postural  sense  can  invariably 
be  improved,  sometimes  to  a  miraculous  extent.  The 
improvement  occurs  without  any  apparent  change  in 
the  lesions.  I  observed  it  occur  once  in  spite  of  an  ad- 
vance in  the  lesions.  It  is  partially  independent  of  the 
lesions.  The  postural  thresholds,  therefore,  seldom  indi- 
cate with  precision  the  severity  of  the  structural  change; 


CHAPTER  IV 

RESULTS  OF  THE  SYPHILITIC  LESIONS 

3.  DISTURBANCES   OF  ATTITUDE   AND   MOVEMENT 

The  changing  and  maintaining  of  attitude.  Attitude  expressive  of  the 
motor  tendencies  that  we  desire  and  of  those  that  are  unconsciously 
evoked  by  the  mental  state.  The  impossibility  of  maintaining  an 
immovable  posture.  Normal  swaying.  Tabetic  swaying.  Rom- 
berg's  sign.  The  tabetic  attitude.  Effect  of  blindness,  psycho- 
therapy and  mental  states  on  the  tabetic  attitude.  The  tabetic  at- 
titude a  consequence  not  only  of  the  lesions  but  also  of  the  men- 
tal state.  Ataxic  movements.  Controversy  regarding  the  cause 
of  ataxia.  Importance  of  the  constituent  parts  of  the  muscular 
apparatus  in  coordination.  Postural  sense  loss  not  parallel  to 
ataxia.  Reflex  defect  not  necessarily  associated  with  ataxia. 
Onset  and  course  of  ataxia.  Fatigue,  fear  and  shock  as  precipi- 
tants  of  ataxia.  The  ataxic  moment.  The  relation  of  ataxia  to 
the  tabetic  lesions.  Psychic  control  of  coordination.  The  ratio 
between  effort  and  accomplishment  in  movement.  Voluntary 
movement  the  resultant  of  the  desired  and  of  the  unconsciously 
evoked  postural  images.  The  interaction  of  voluntary  and  of  re- 
flex movement.  Psychic  activity  masking  reflex  defect  in  volun- 
tary movement  throughout  the  preataxic  stage.  Ataxic  complexes. 
Coefficient  of  ataxia.  The  reciprocal  relations  of  ataxia  and  the 
mental  state.  The  amount  of  disturbance  of  attitude  and  move- 
ment mainly  a  measure  not  of  the  structural  changes  but  of  the 
degree  of  the  failure  of  conscious  control  of  movement  to  com- 
pensate for  the  tabetic  defect  in  the  reflex  mechanism.  The  sur- 
render or  so-called  "paralytic"  stage. 

IN  infancy,  we  consciously  acquire  power  to  alter  the 
relation  of  the  various  bony  levers  of  the  skeleton  to 
one  another  and  to  the  horizon.  We  learn  first  to  hold 
up  our  heads,  then  to  sit  erect,  and  last  to  stand.  In 
adult  life,  if  we  merely  desire  to  change  our  attitude,  say, 

61 


62  LOCOMOTOR  ATAXIA 

from  sitting  to  the  erect  posture,  the  act  automatically 
follows. 

In  maintaining  an  attitude,  we  conserve  the  position 
of  the  skeletal  levers  against  a  constant  force  acting  in 
a  constant  direction,  the  force  of  gravity.  The  tone  of 
the  muscles  whose  action  is  opposed  to  that  force  is  kept 
high  that  these  muscles  may  remain  taut;  and  the  tone 
of  their  antagonists  low,  that  those  may  be  lax.  The 
position  of  the  head  reflexly  determines  that  of  the  rest 
of  the  body. 

The  posture  does  not  exclusively  reflect  the  desire. 
The  mood,  the  emotion,  the  mental  state  at  the  moment 
it  is  assumed,  have  motor  attributes  of  which  we  are 
unconscious,  but  with  which  the  desired  posture  must  be 
compounded.  The  influence  of  the  mental  state  on  pos- 
ture is  universally  recognized;  everyone  can  distinguish 
the  attitude  of  the  tired  from  that  of  the  fresh;  of  the 
apathetic  from  the  alert;  of  the  depressed  from  the 
joyous.  Indeed,  mental  states  are  often  defined  by  their 
resulting  attitude:  thus,  the  sad  droop;  the  craven  are 
"spineless"  and  "weak-kneed";  the  brave  are  upright; 
and  so  forth.  The  posture  attained  is  the  resultant 
of  both  the  desired  and  the  unconscious  motor  tenden- 
cies. 

Even  with  an  absolutely  normal  motor  mechanism,  we 
cannot  maintain  an  immovable  posture.  Soldiers  and 
others  may  be  trained  to  stand  with  the  feet  alongside 
and  parallel  to  one  another,  apparently  motionless,  but 
a  writing  point  fixed  to  the  head  of  the  most  steady,  in- 
variably records  fourteen  to  sixteen  oscillations  per 
second;  and  if  the  investigated  person  be  warned  to 
expect  a  sound  from  the  right  or  from  the  left,  the  oscil- 
lations become  directed  towards  the  expected  sound.  The 


RESULTS  OF  SYPHILITIC  LESIONS          63 

oscillations  are  aggravated  on  closing  the  eyes  and  in 
constrained  attitudes,  such  as  standing  on  one  foot,  or 
bending.  These  oscillations,  usually  imperceptible  to 


SAD 


TIRED 


CONFIDENT 


TIMID 

FIG.  36. — "The  mood,  the  emotion,  the  mental  state,  at  the  moment — havs 
motor  attributes  of  which  we  are  unconscious. " 

unaided  vision,  become  evident  in  the  tabetic.    He  sways 
obviously  when  he  stands  with  closed  eyes  (Romberg's 
sign). 
Swaying  is   first   evident   in  the   tabetic  only  when 


EVES  SHUT  OPEN. 

FIG.  37. — Tracing1  of  lateral  swaying  in  a  normal  person  showing  the  gradual 
increase  of  the  extent  of  the  swaying  after  the  eyes  are  closed.  (Graham 
Brown.) 

*The  Knauer-Maloney  cephalograph  records  the  resultants  of  the 
swaying  in  all  planes.  I  give  no  examples  of  its  tracings  for  I  find 
some  of  the  oscillations  it  records  are  due  to  a  mechanical  defect  in 
the  machine,  a  defect  which  is  easy  to  remedy  but  which  I  have  not 
yet  cured.  The  present  type  of  the  machine  is  of  value  merely  for 
clinical  work  but  not  for  scientific.  Only  the  tracings  taken  by  the 
same  observer  with  the  same  cephalograph  are  comparable.  Those  who 
may  be  interested  in  its  design  will  find  it  fully  described  and  illus- 
trated in  The  Journal  of  Nervous  and  Mental  Diseases,  Sept.,  1914. 


64  LOCOMOTOR  ATAXIA 

• 

he  is  standing  with  closed  eyes,  in  constrained  attitudes. 
Under  similar  circumstances,  many  who  are  not  tabetic 
may  be  seen  to  sway.  There  is  no  limit  of  non-tabetic 
instability,  no  threshold  of  Rombergism.  But  usually 


FIG.  38. — "To  counteract  the  dis- 
turbance of  balance,  the  erect 
tabetic  has  recourse  first  to  one 
stick,  the  tripod  stage"  .  .  . 
(Montefiore  Hospital  Case.) 


FIG.  39.— "To  counteract  the 
disturbance  of  balance  the 
erect  tabetic  has  recourse — 
then  to  two  sticks,  the  quad- 
ruped stage. "  (Montefi- 
ore Hospital  Case.) 


the  non-tabetic  instability  is  slight;  develops  when  the 
constrained  posture  is  long  maintained;  and,  on  succes- 
sive examinations,  does  not  increase.  Tabetic  instability 
is,  as  a  rule,  immediately  apparent  when  the  constrained 
posture  is  assumed,  is  aggravated  by  continuance  of 
the  posture,  and  on  reexamination  discloses  a  tendency 
to  increase.  This  tendency  to  increase,  I  think,  is  the 


RESULTS  OF  SYPHILITIC  LESIONS 


65 


chief  distinction  between  doubtful  tabetic  and  non-tabetic 
swaying.  Knauer  and  Maloney  devised  a  cephalograph  l 
which  graphically  records  head  movements  in  three 
planes.  By  its  use,  the  extent  of  the  patient's  swaying 
is  ascertained  and  recorded 
when  he  is  first  examined.  By 
comparing  the  first  with  sub- 
sequent records,  increase  in 
swaying  can  be  detected.  A 
diagnosis  of  Rombergism  can 
thus  be  early  reached. 

Tabetic  swaying,  at  first 
obvious  only  in  constrained 
attitudes,  is  next  evident  in 
normal,  then  in  broad  base, 
and  finally  in  supported,  atti- 
tudes. It  later  may  occur  suc- 
cessively in  these  attitudes 
even  when  the  eyes  are  open. 
The  wider  the  arc  of  the  sway- 
ing, the  broader  must  be  the 
tabetic's  base,  if  he  is  to  re- 
main erect.  He  may  sway 
through  an  arc  so  wide  that  to 
enlarge  his  base  he  moves  his 
feet;  he  reels.  Reeling  on  eye 


FIG.  40. — Further  development 
of  the  "quadruped  stage." 
The  blurring  of  the  picture 
was  due  to  the  patient's 
swaying.  (Montefiore  Hos- 
pital Case.) 


closure    in    the    usual    erect  posture  is  always  patho- 
logical. 

To  counteract  this  disturbance  of  balance,  the  erect 
tabetic  has  recourse  first  to  one  stick,  the  tripod  stage, 
and  then  to  two  sticks,  the  quadruped  stage.  He  may 
ultimately  become  unable  to  assume  and  to  maintain 

*Made  by  the  Medical  Machinery  Company,  Detroit,  Michigan. 


66 


LOCOMOTOR  ATAXIA 


any  attitude  except  the  recumbent.  This  deterioration 
of  attitude  may  halt  at  any  stage.  The  courageous  can 
always  maintain,  although  distortedly,  an  erect  posture. 
The  timid  surrender  after  passing  through  the  tripod 
and  quadruped  stages,  and  become  chair-ridden  and 
finally  bed-ridden. 

The  blind  tabetic,  as  a  rule,  conserves  his  power  to 

stand  erect.  A  tabetic  who 
has  lost  that  power  and 
who  becomes  blind  may 
then  spontaneously  regain 
it.  Under  the  influence  of 
psychotherapy,  the  recum- 
bent tabetic  may  be  made  to 
rise  again  and  to  stand 
steadily  even  with  closed 
eyes.  Equilibration  is  more 
difficult  in  fear,  fatigue  and 
depression,  in  the  seeing 
than  in  the  blind,  in  the  un- 
trained than  in  the  trained. 
If  a  blindfolded,  seated 
tabetic,  whose  feet,  back 
and  head  are  well  and  com- 
fortably supported,  attempt 

FIG.  41. — "The  courageous  can  al- 
ways maintain,  although  dis-    to   maintain   his   arms   out- 
tortedly    an   erect   posture."    stretched  in  front  of  him,  the 

(Montefiore  Hospital  case.) 

arms  may  fall,  one,  perhaps, 

faster  than  the  other.  Sometimes  the  fall  is  slow  and 
steady.  Usually  it  is  somewhat  and  increasingly  un- 
steady; the  arms  may  oscillate  more  and  more  widely, 
till  the  tabetic  ceases  effort  and  lets  them  drop.  The 
tabetic  to  whom  the  unsteadiness  is  inappreciable  not 


RESULTS  OF  SYPHILITIC  LESIONS          67 

rarely  is  amazed  to  see  his  arms  fallen,  which  he  sup- 
posed were  still  outstretched. 

I  have  many  times  tested  the  appreciation  of  change 
of  posture  at  the  shoulder,  in  cases  in  which  spontaneous, 
unnoticed  fall  of  the  arms  occurred.  For  movement  at 
approximately  the  same  rate  as  the  fall,  thresholds  of 
less  than  ten  degrees  were  almost  invariable.  Indeed, 
it  was  usually  difficult  to  move  the  shoulder  of  such  a 
tabetic  slowly  enough  to  prevent  his  detecting  a  change 
through  an  arc  of  more  than  three  or  four  degrees.  A 
tabetic  with  a  threshold  of  only  a  few  degrees  may  be 
ignorant  of  a  movement  through  an  arc  of  nearly  ninety, 
of  a  movement  perhaps  a  thousand  per  cent  greater  than 
his  demonstrable  postural  threshold. 

This  curious  phenomenon  is  due  to  the  habit  which  the 
tabetic  acquires  of  not  attending  to  the  postural  images 
which  accompany  movement.  The  few  feeble  and  delayed 
postural  impulses,  transmitted  from  the  section  of  the 
muscular  apparatus  which  corresponds  to  the  diseased 
fibers  in  posterior  root  or  in  vestibular  nerve,  excite 
feeble,  imperfect  and  delayed  postural  images.  Such 
defective  images  mislead  and  delude  the  tabetic  in  move- 
ment. He  sees  simultaneously  many  objects,  every  one  of 
which  confirms  his  faith  in  the  impeccability  of  his 
visual  information.  He  therefore  relies  on  his  visual 
images  to  judge  and  guide  his  movements ;  and  he  ignores 
and  suppresses  the  misleading  postural  after-images. 
Hence,  unless  he  consciously  concentrates  his  attention 
on  these  neglected  after-images,  he  is  unaware  of  his 
posture  when  his  eyes  are  shut.  This  suppression  is  not 
a  phenomenon  peculiar  to  postural  images.  Those  who 
see  double  suppress  the  false  image ;  those  who  are  deaf 


68  LOCOMOTOR  ATAXIA 

suppress  unintelligible  sounds.    Suppression  of  what  is 
undesired  is  a  normal  mental  reaction. 

Suppression  of  any  image  tends  to  suppress  those 
habitually  associated  with  it.  The  suppression  of  the 
postural  images  of  the  outstretched  arms  tends  to  sup- 
press also  the  motor  equivalent  of  those  postural  images, 
the  muscular  action  necessary  to  maintain  the  posture. 
The  desire  to  maintain  the  posture  must  prevail  over  the 
unconscious  tendency  to  suppress  it,  or  the  arms  fall. 
The  length  of  the  time  the  posture  is  maintained  affords 
a  measure  of  the  dominance  of  the  desired  over  the 
unconscious  motor  tendencies. 

But  these  unconscious  motor  tendencies  arise  also 
from  sources  other  than  the  direct  suppression  of  the 
essential  motor  images  through  the  suppression  of  their 
peripherally  excited  postural  equivalents.  The  more  a 
tabetic  relies  on  vision  the  more  does  absence  of  vision 
leave  him  with  a  consciousness  of  sensory  perception 
analogous  to  that  present  in  night  terrors.  The  lack 
of  peripherally  excited  postural  images  from  the  misty 
consciousness  of  light  sleep  gives  rise  to  the  sensation 
of  falling,  or  to  the  cognate  sense  of  inability  to  move; 
and  engenders  sudden  great  fear.  The  suppression  of 
the  imperfect  postural  after-images  by  the  tabetic,  on  eye 
closure,  leads  to  fear.  Fear  inhibits  all  associations  and, 
therefore,  causes  swaying,  reeling,  and  falling.  Occa- 
sionally, instead  of  swaying,  the  tabetic  collapses  as  if 
suffering  from  hysterical  paralysis.  Indeed,  fear  in  the 
tabetic  may  be  the  dominant  element  in  the  lack  of 
equilibration.  Thus,  Dercum  reports  a  case  of  a  blind 
tabetic  negro  who  could  stand  steadily  so  long  as  his  eyes 
were  open,  but  who  reeled  and  fell  when  his  eyelids 
closed  over  his  sightless  eyes. 


RESULTS  OF  SYPHILITIC  LESIONS          69 

But  the  characteristic  of  voluntary  movement  in  tabes 
is  its  disorder,  its  ataxia.  Normal  voluntary  movements 
are  thrifty  in  force,  accurate  in  direction,  regular  in 
order,  uniform  in  rhythm  and  precise  in  extent.  Move- 
ments lacking  this  composite  quality  to  a  degree  evident 
to  the  unaided  eye  are  said  to  be  ataxic. 

Since  ataxia  was  first  recognized,  neurologists  have 
conducted  researches  and  controversies  upon  its  cause. 
Theories  of  ataxia  have  succeeded  one  another  like  de- 
crees of  fashion.  Brown-Sequard  (1861)  taught  the 
spinal  or  reflex  theory.  Ley  den  (1863  et  seq.)  founded 
his  sensory  theory  on  his  observations  that  ataxia  may 
first  appear  in  a  limb  where  loss  of  cutaneous  sensibility 
is  evident,  and  that  the  increase  of  the  ataxia  may  be 
roughly  parallel  to  that  of  this  sensory  loss.  Charcot 
agreed  with  Leyden.  Erb  (1859),  Friedreich  (1879),  and 
others  pointed  out  that  ataxia  could  occur  without  loss 
of  common  sensibility.  Jendrassik  (1888)  and  Kaymond 
(1897)  stoutly  maintained  that  neither  sensory  nor  mo- 
tor, but  cerebral  causes  underlay  ataxia.  Goldscheider 
(1889)  emphasized  the  importance  of  postural  sense  loss; 
Frenkel  and  Forster  and  others,  of  loss  of  tone  in  the 
muscles;  Dejerine  and  Egger,  of  loss  of  the  vibration 
sense  in  the  bones.  Some  have  cocainized  the  joints  and 
blamed  the  loss  of  sensibility  in  the  articular  cartilages ; 
others  have  removed  or  cocainized  the  skin  and  have 
absolved  it  from  contributing  to  ataxia. 

In  all  movement,  alterations  occur  in  the  pressure  at 
the  points  of  contact  on  the  articular  surfaces  of  the 
moving  joint,  and  in  the  tension  of  the  implicated  liga- 
ments, tendons  and  muscles,  and  of  the  skin  which  covers 
them,  and  of  the  bones  into  which  they  are  inserted. 
These  alterations  give  rise  to  stimuli  some  of  which  are 


70  LOCOMOTOK  ATAXIA 

sentient,  some  non-sentient.  The  sentient  stimuli  under- 
lie postural  appreciation,  and  with  visual  impulses  afford 
a  basis  for  comparing  the  attained  with  the  desired 
posture.  A  loss  of  sensibility  in  any  one  of  these  com- 
ponent parts  of  the  muscular  apparatus  disturbs  postural 
sense,  according  to  the  degree  of  the  loss,  and  to  the 
power  of  the  sensibility  resident  in  the  other  parts  to 
compensate  for  that  loss. 

Of  the  component  parts  of  the  muscular  apparatus, 
the  skin  seems  to  be  least  indispensable  to  coordination, 
for  anesthetizing  with  cocain  and  even  removal  of  the 
skin  do  not  greatly  disturb  coordination.  As  large  joints 
are  more  sensitive  to  movement  than  small,  although  a 
small  has  a  relatively  greater  articular  surface  than  a 
large  joint,  the  joint  cartilages  do  not  play  the  major 
role  in  coordination.  The  most  important  element  of  the 
muscular  apparatus  in  the  function  of  coordination  is 
the  sensory  receptors  in  the  muscles  and  tendons. 

In  tabes,  ataxia  may  or  may  not  be  parallel  to  the 
postural  sense  loss.  There  may  be  postural  sense  loss 
without  evident  ataxia.  Indeed,  such  loss  is  not  uncom- 
monly detected  during  the  preataxic  stage.  The  insig- 
nificant amount  of  ataxia  seen  associated  in  thalamic 
lesions  with  loss  of  all  forms  of  sensibility,  including 
that  of  posture,  further  shows  the  inadequacy  of  exclu- 
sive sensory  theories. 

In  consequence  of  the  tabetic  lesions  affecting  the  non- 
sentient  stimuli,  measurable  disturbance  of  the  reflex 
coordinating  mechanism  results,  to  a  degree  depending 
upon  the  site,  severity,  and  rapidity  of  development  of 
the  lesions,  and  upon  the  compensatory  activity  of  the 
intact  reflexes.  The  disturbance  may  by  graphic  meth- 
ods be  demonstrable  before  ataxia  is  apparent,  and  after 


RESULTS  OF  SYPHILITIC  LESIONS         71 

ataxia  has  been  banished  by  suitable  therapy.  The  reflex 
theory  is,  therefore,  inadequate  to  explain  ataxia. 

The  structural  changes  in  the  cerebral  cortex  which 
Jendrassik  described  and  which  he  thought  substantiated 
his  cerebral  theory,  have  been  shown  to  be  not  only  in- 
constant but  exceptional  in  tabes. 

Yet  each  of  these  theories  contains  part  of  the  truth 
and  all  together  contain  most  of  it.  In  tracing  the  course 
of  tabetic  ataxia,  I  shall  emphasize  the  factors  which 
govern  it  so  that  a  clear  idea  of  its  production  may 
accompany  its  description. 

Ataxia  is  first  noticeable  in  a  limb  or  limbs,  commonly 
in  the  lower,  not  in  the  upper;  but  ataxia  of  the  limbs 
does  not  occur  without  incoordination  of  the  head  and 
trunk. 

Typically  the  onset  of  ataxia  is  insidious:  the  tabetic 
notices  he  is  more  easily  fatigued;  he  has  difficulty  in 
walking  in  the  dark;  he  falls  into  the  basin  if  he  closes 
his  eyes  while  washing ;  he  no  longer  feels  the  ground  as 
before;  he  feels  as  if  he  walked  on  some  thick  yielding 
surface,  such  as  rubber,  or  felt,  or  cotton  wool;  he  is 
uncertain  in  descending  stairs  or  inclines.  Uncertainty, 
at  first  intermittent,  becomes  more  and  more  continuous 
until  movement  is  scarcely  possible  without  meticulous 
care.  This  care  implies  increase  of  effort;  misguided, 
ill-judged  effort  causes  his  uncertainty  to  grow  with 
every  movement.  The  gait  becomes  strutting,  the  move- 
ment jerky,  chaotic  and  extravagant ;  the  feet  are  banged 
upon  the  ground ;  and  the  trunk  is  held  stiffly  at  awkward 
angles. 

Sudden  exacerbation  may  occur,  which  the  ataxic  at- 
tributes to  a  definite  incident,  a  chill,  a  fall,  a  fright,  or 
overwork.  After  such  an  exacerbation,  improvement 


72  LOCOMOTOR  ATAXIA 

may  occur  but  the  ataxia  seldom  decreases  to  the  degree 
which  existed  before  the  incident  happened. 

Instead  of  insidiously  progressing  the  ataxia  may  ad- 
vance with  fulminating  rapidity.  Such  cases  have  been 
especially  reported  by  the  French  neurologists  (ataxie 
d'emblee). 

Ataxia  may  begin  suddenly  and  be  from  its  commence- 
ment of  severe  degree.  Gowers  (p.  366)  records  a  case 
in  which  severe  ataxia  developed  in  twenty-four  hours. 
Ataxia  may  precipitately  appear  after  fatigue.  Ingle- 
rans  reports  that  Rosalie  X,  in  November,  1891,  ran 
after  a  tramcar,  on  -reaching  which  she  felt  ill.  At 
the  end  of  her  journey,  when  she  rose  to  leave  the  car, 
her  legs  would  scarcely  support  her.  She  reeled  to  her 
home  where  her  ataxia  thereafter  confined  her. 

Dr.  James  Taylor  had  under  his  care  at  the  National 
Hospital,  London,  a  tabetic  who,  while  on  duty  as  a 
policeman,  after  a  long  and  swift  chase  captured  a 
criminal.  While  the  captive  was  being  escorted  by  others 
to  prison,  the  tabetic  policeman  was  being  carried  to  the 
hospital,  incapable  of  effective  movement,  owing  to  an 
explosive  onset  of  ataxia. 

Besides  fatigue,  fear  also  may  act  as  a  precipitant  of 
ataxia.  In  addition  to  the  following  example,  I  have 
published  another  [  Journal  of  Nervous  and  Mental  Dis- 
ease, Vol.  40,  No.  11,  1913]  and  seen  a  third. 

An  elderly  gentleman  decided,  not  without  misgiving, 
to  take  for  the  first  time  in  his  life,  a  short  holiday  in 
Europe.  He  was  visiting  a  cave,  which  was  lit  by  elec- 
tricity. The  patient  told  me  he  did  not  like  the  escapade ; 
to  go  under  the  earth  alone  with  foreigners  seemed  to 
him  hazardous.  Suddenly  all  the  lights  went  out.  The 
darkness  was  absolute.  His  worst  fears  seemed  about 


RESULTS  OF  SYPHILITIC  LESIONS          73 

to  be  realized.  He  stretched  out  a  panic-stricken  foot 
for  the  next  step,  and  felt  nothing.  Then  he  collapsed, 
was  gently  carried  out  of  the  cave  and  tended  in  the  local 
hospital.  He  had  completely  lost  his  power  of  walking. 
When  I  saw  him  two  weeks  later  he  had  Argyll-Robert- 
son pupils,  no  knee-jerks,  and  other  classical  signs  of 
tabes,  together  with  an  incapacitating  degree  of  ataxia. 

I  have  also  recorded  (loc.  cit.  supra)  three  cases  in 
which  stumbles  precipitated  the  tabetic  from  coordination 
into  ataxia. 

The  ataxia  in  such  cases  appears  suddenly,  at  a  defi- 
nite, ascertainable  moment  which  we  may  call  the  ataxic 
moment.  Before  the  ataxic  moment  movement  is  ap- 
parently normal ;  after,  chaotic. 

In  absence  of  all  other  ascertainable  causes,  we  must 
attribute  the  bizarre  onset  of  the  ataxia  in  these  cases 
to  the  fatigue  or  fright  or  trivial  mishap  which  immedi- 
ately preceded  it.  Without  this  inciting  occurrence,  the 
ataxia  would  presumably  have  later  developed  gradually, 
imperceptibly  almost,  as  is  its  habit.  In  cases  such  as 
these  there  is  no  question  of  alteration  in  the  lesions. 
The  effect  is  immediate  and  entirely  mental. 

When  ataxia  develops  under  observation  its  first  ap- 
pearance may  or  may  not  coincide  with  a  detectable 
advance  in  the  structural  changes.  With  the  progress 
of  the  ataxia  the  lesions  may,  but  usually  do  not,  increase. 
Increase  of  the  lesions  may,  or  may  not,  give  rise  to 
increase  of  the  ataxia.  An  ataxic  under  my  care  lost 
the  right  third  and  fourth  lumbar  roots  following  a 
salvarsan  injection.  Before  this  accident  I  had  meas- 
ured his  postural  sense  in  the  right  lower  limb  and  had 
taken  several  records  of  his  gait.  No  detectable  change 
happened  after  the  accident. 


74  LOCOMOTOR  ATAXIA 

Daily  variations  occur :  the  ataxia  is  greater  in  fatigue 
than  in  freshness,  in  despondency  than  in  cheerfulness, 
in  pain  than  in  comfort,  in  fear  than  in  calm. 

Exerted  in  the  form  styled  reeducation,  or  as  hypnosis, 
or  as  Christian  Science;  or  through  the  medium  of  me- 
chanical forces  such  as  electricity,  or  of  chemical  sub- 
stances such  as  salvarsan,  or  of  well  advertised  fetishes 
such  as  rings,  or  belts,  or  boots,  psychotherapy  may  de- 
crease the  ataxia.  The  improvement  lasts  as  long  as  the 
benign  psychic  influence  is  maintained.  The  degree  of 
improvement  may  be  such  as  to  induce  a  return  to  the 
preataxic  stage. 

Ataxia  may  be  absent  in  presence  of  typical  tabetic 
lesions;  an  increase  in  those  lesions  is  not  always  fol- 
lowed by  an  increase  in  the  ataxia;  without  evident 
alteration  in  the  lesions,  ataxia  may  develop  and  may 
progress ;  under  the  influence  of  psychotherapy  or  blind- 
ness, ataxia  may  retrogress ;  transient  mental  states  may 
noticeably  increase  or  diminish  the  ataxia.  Ataxia  is, 
therefore,  not  wholly  dependent  upon  the  tabetic  struc- 
tural changes.  It  is  indubitably  a  consequence  of  the 
tabetic  lesions  but  not  an  invariable  one;  it  is  a  conse- 
quence to  a  certain  extent  indirect  and  to  that  extent 
avoidable  and  remediable. 

A  reflex  is  not  subject  to  such  variations.  Its  con- 
stancy and  infallibility  are  among  its  chief  characteris- 
tics. Neither  does  the  effectivity  of  a  group  of  reflexes 
vary  without  cause.  Hence,  the  variations  in  ataxia 
which  result  from  emotions,  moods,  psychotherapy  and 
blindness  must  be  due  to  a  component  of  coordination 
other  than  the  reflex  structural  mechanism  which  some 
allege  is  the  sole  mechanism  concerned. 

The  only  influence  which  is  subject  to  mood,  to  environ- 


RESULTS  OF  SYPHILITIC  LESIONS          75 

ment  and  to  physical  conditions,  which  is  greater  in  the 
blind  than  in  the  seeing  and  in  the  trained  than  in  the 
untrained,  is  a  psychic  influence.  The  efficiency  of  the 
reflex  coordinating  mechanism  can  be  enhanced  and  di- 
minished during  voluntary  movement  by  psychic  power. 

When  we  desire  to  move,  we  wish  to  change  from  an 
existing  to  a  new,  the  desired,  posture.  In  the  transit 
we  assume  intermediate  postures  which,  if  we  move  per- 
fectly, are  those  that  render  the  movement  accurate  in 
direction,  and  precise  in  extent. 

Normally,  in  acquiring  a  new  movement,  we  watch  our 
crude  attempts.  Watching  reduces  visual  distraction 
and  focusses  attention  upon  the  movement.  When  the 
movement  errs  in  direction  or  in  extent,  we  perceive 
the  fault.  By  concentrating  attention  upon  the  faultless 
postures,  we  facilitate  associations  among  them  and  sup- 
press the  associations  of  erring  postures  we  may  inad- 
vertently attain.  Thus,  we  learn  to  assume  in  succession 
the  optimal  postures  between  the  existing  and  the  ulti- 
mate posture  desired. 

The  more  often  the  same  postural  images  are  linked 
together  the  more  inevitable  is  their  association.  Prac- 
tice engraves  these  optimal  postures  and  their  sequence 
on  memory.  After  an  interval  which  varies  with  the 
individual  and  with  the  complexity  of  the  movement,  the 
eliciting  of  the  desired  in  association  with  the  existing 
postural  images  excites  in  series  the  images  which,  link 
them  and  suppresses  all  images  alien  to  the  series. 

Practice  decreases  the  need  for  conscious  attention^ 
visual  fixation  becomes,  therefore,  less  and  less  neces- 
sary. Practice  lessens  the  need  for  correction;  visual 
control,  therefore,  becomes  superfluous.  Finally,  vision 
is  dispensed  with  in  the  performance  of  the  movement 


76  LOCOMOTOR  ATAXIA 

and  remains  only  as  a  potential  critic  of  the  completed 
act.  The  amount  of  visual  direction  which  a  movement 
requires  is  an  index  of  the  amount  of  attention,  of  men- 
tal effort,  it  involves.  Moreover,  gross  movements  such 
as  walking,  so  long  as  they  need  effort,  so  long  as  they 
are  visually  directed,  are  clumsy. 

The  ratio  between  the  needed  effort  and  the  accom- 
plished movement  varies  as  the  mental  state.  In  un- 
favorable states,  effort  may  be  spared  at  the  expense 
of  the  movement;  or,  in  spite  of  maximal  effort,  move- 
ment may  be  imperfect.  Thus,  movements  are  slow  in 
fatigue,  in  depression  and  in  fear;  and  beside  the  rate, 
the  strength  diminishes  and,  especially  in  fear,  the 
rhythm  suffers.  As  the  musculature  is  an  organ  of 
expression,  of  adaptation,  mental  states  and  emotions 
may  excite  and  inhibit  postural  images ;  thus,  the  process 
of  thought  in  Gallic  races  is  accompanied  by  gesticula- 
tions, often  more  eloquent  than  words ;  and,  in  the  tradi- 
tional snail-like  progress  of  boys  on  their  way  to  school, 
inhibition  is  evident. 

In  a  voluntary  movement  the  psychic  resultant  of  the 
desired  and  of  the  unconsciously  provoked  postural  im- 
ages excites  the  motor  cells  of  the  Bolandic  area  in  the 
cerebral  cortex.  The  effect  of  this  excitation  is  conveyed 
by  the  pyramidal  tract  fiber  to  motor  cells  in  the  cord, 
or  medulla,  or  pons.  These  motor  cells  we  considered 
first  as  the  final  cell  stations  of  motor  reflex  activity. 
Upon  these  final  common  cells,  psychic  and  reflex  influ- 
ences act  conjointly,  affecting  them  in  similar  ways  (page 
43).  The  result  of  this  conjoint  action,  the  motor  energy 
liberated  in  the  cell,  passes  by  a  single  path,  the  axon  of 
the  final  common  cell,  to  voluntary  muscle,  there  to  ex- 


RESULTS  OF  SYPHILITIC  LESIONS          77 

cite  changes  which  externalize  the  reflex  and  psychic  ac- 
tivity as  muscular  action. 

In  tabes,  throughout  the  preataxic  stage,  the  desire  to 
move  excites  images  adequately  to  procure  orderly  move- 
ment: the  intensity  of  the  excitation  of  the  motor  cortex 
in  the  brain  compensates  for  faulty  reflex  action  in  the 
cord.  The  greater  the  lesions,  the  more  effort  is  needed 
to  maintain  this  compensation;  ceteris  paribus,  the 
sooner  ataxia  develops:  ataxia  first  appears  in  that  one 
of  a  pair  of  limbs  which  shows  the  most  advanced  lesions. 
The  less  the  initial  mental  capacity,  the  more  powerful 
is  the  ataxic  tendency  of  the  lesions;  the  more  trivial 
is  the  defect  which  is  capable  of  causing  ataxia ;  and  the 
shorter  is  the  preataxic  stage.  The  less  automatic  a 
movement  is,  the  more  effort  is  needed  for  its  accom- 
plishment, and  the  less  it  tends  to  persist  coordinate. 
Thus  the  visually  directed  arm  movements  are  more 
easily  and  more  speedily  decomposed  than  the  automatic 
movements  of  walking.  Walking  is  more  difficult  on 
stairs  or  on  inclines  than  on  a  level  surface.  In  the 
order  of  the  effort  required  for  its  performance  under 
different  circumstances,  walking  becomes  faulty. 

As  fatigue  and  fear  develop,  greater  and  greater  effort 
is  needed  to  evoke  with  sufficient  intensity  the  desired 
postural  images  so  that  they  will  dominate  the  uncon- 
scious motor  tendencies  and  will  stimulate  the  motor 
cortex  to  a  degree  which  compensates  for  the  incoordi- 
nating  tendencies  of  the  reflex  mechanism. 

All  the  daily  influences  which  contribute  to  fear, 
fatigue,  and  other  unfavorable  mental  states,  are  influ- 
ences prejudicial  to  movement  and  constitute  so  many 
incentives  to  ataxia,  so  many  ataxic  complexes. 


78  LOCOMOTOR  ATAXIA 

The  liability  to  ataxia  may  be  expressed  by  the  ratio 
of  all  the  ataxic  tendencies  to  the  coordinating  power, 

Ataxic  tendencies 


Coefficient  of  ataxia  = 


Coordinating  powBr. 
Of  these  tendencies,  the  lesions  may  practically  be  con- 
sidered as  a  constant :  the  ataxic  complexes,  as  a  variable 
whose  value  determines  the  appearance  and  the  degree 

s   of  ataxia.     The  coordinating  power  depends  upon  the 

» 

integrity  of  the  reflex  and  cerebral  mechanisms  of  move- 
ment and  upon  the  effectiveness  of  the  psychic  control 
over  these  mechanisms. 

So  long  as  the  denominator  of  this  formula  is1  greater 
than  the  numerator,  that  is,  so  long  as  the  coefficient  of 
ataxia  is  less  than  unity,  so  long  endures  the  preataxic 
stage;  so  long  is  movement  coordinate;  so  long  is  re- 
pression of  the  ataxic  tendency  adequate.  When  the 
numerator  and  the  denominator  are  equal,  the  coefficient 
of  ataxia  is  unity;  and  the  ataxic  threshold  is  almost 
reached.  To  this  value  the  coefficient  had  uhsuspectedly 
attained,  just  previous?  to  the  fatigue,  stumbles  and 
frights  which  at  the  ataxic  moment  precipitated  the  cases 
of  acute  onset  I  mentioned  (pp.  72  and  73),  from  coordi- 
nation to  ataxia. 

Preataxic  tabetic^  fatigue  often  and  readily,  and  fear 
a  thousand  times  a  day;  blind  tabetics  stumble  in  their 
blindness  more  than  any  other  preataxic  tabetic;  yet, 
until  the  ataxic  moment,  ataxia  does  not  develop.  In  all 
previous  fatigue,  frights  and.  stumbles,  the  tabetic  had 
not  reached  the  ataxic  threshold,  the  coefficient  was 
safely  below  unity;  and  any  increase  in  its  value  which 
then  resulted  was  inadequate  to  exert  a  visible  effect 
upon  coordination.  The  nature  and  intensity  of  the 
occurrence  which  incites  to  ataxia  may  in  part  determine 


79 

its  effect,  but  the  main  determinant  is  the  mental  state 
at  the  ataxic  moment.  Upon  the  mental  state  depends 
the  degree  of  the  shock  which  the  occurrence  induces. 
The  integrity  of  the  coordinating  mechanism  determines 
the  power  of  the  shock  to  precipitate  ataxia. 

So  long  as  the  desired,  the  consciously  evoked  postural 
images,  can  dominate  the  unconscious;  and  so  long  as 
this  dominance  is  adequate  to  excite  through  the  cells 
of  the  Bolandic  area,  a  reproduction  of  the  desired 
postures  strong  enough  to  mask  the  reflex  defect  of 
tabes,  movement  remains  coordinate  in  spite  of  that 
reflex  defect. 

We  have  seen  that  the  impulses  arising  from  the 
muscular  apparatus  during  a  movement  excite  images  of 
posture  in  the  cerebral  cortex.  The  resultant  of  these 
peripherally  excited  postural  images  we  may  consider 
as-  the  peripheral  reflection  or  after-image  of  the  move- 
ment. There  recurs  (perseverates)  in  the  brain,  after  a 
movement  has  been  accomplished,  a  feeble  image  of  the 
conscious  desire  which  called  it  forth,  an  image  which 
we  may  consider  as-  the.  central  after-image  of  the-  move- 
ment. These  after-images  are  identified  in  the  sphere  of 
the  associations.  Identification  is  the  minimum  associa- 
tion any  image  may  experience.  Neither  survives  nor 
enters  consciousness.  The  central  and  peripheral  after- 
images completely  suppress  or  neutralize  one  another, 
not,  however,  wholly  without  result.  From  their  mutual 
suppression,  a  more  or  less  conscious  feeling  of  content, 
of  balance,  of  proper  accomplishment  ensues :  the  critique 
of  the  movement  is  satisfied.  If  the  mutual  suppression 
be  not  complete,  if  the  peripheral  cannot  neutralize  the 
central  after  image,  the  critique  is  dissatisfied.  Then 
the  movement  is  at  once  reviewed  to  trace  the  cause 


80  LOCOMOTOR  ATAXIA 

of  the  uneasiness,  the  uncertainty,  which  it  has  aroused. 

The  feeble,  delayed  and  imperfect  postural  images 
which  arise  from  the  musculature  in  the  area  of  the 
invaded  roots,  are  inadequate  to  neutralize  the  central 
after-images  to  which  they  should  be  equivalent.  The 
tabetic's  vision  informs  him  that  in  spite  of  his  uncer- 
tainty the  movement  seems  perfect.  The  defective 
peripheral  after-images  perplex  and  distract  him.  He 
must  constantly  reassure  himself  visually  that  his  move- 
ments are  not  as  faulty  as  they  feel.  Hence,  he  relies 
more  and  more  upon  vision  to  tell  him  how  he  moves, 
and  he  obviates  some  of  his  uncertainty  by  suppressing 
the  false  information  from  his  peripheral  after-images 
of  movement. 

During  this  stage  of  replacing  postural  images  (after- 
images of  movement)  by  visual  images  as  criteria  of 
movement,  of  substituting  a  conscious  critique  for  one 
which  was  chiefly  unconscious,  the  tabetic  experiences 
added  effort  in  moving.  This  greater  effort  is  not 
wholly  attributable  to  the  constant  watch  he  now  main- 
tains. Visual  substitution  is  accompanied  by  conscious 
suppression  of  the  misleading  peripherally  excited  postu- 
ral images,  the  after  images  of  movement.  Their  sup- 
pression tends  to  suppress  all  their  motor  equivalents, 
because  the  suppression  of  any  one  of  a  series  of  images 
habitually  associated  tends  to  suppress  the  whole  series, 
together  with  the  associations  of  the  series.  To  over- 
come this  unconscious  endeavor  to  suppress  the  move- 
ment, greater  effort  is  needed  to  perform  it.  The  fatigue 
thus  entailed  is  redoubled  by  the  inhibitory  influence 
exerted  on  movement  through  the  fear  induced  by  in- 
creasing vigilance  and  by  growing  uncertainty. 

When  vision  has  been  substituted  for  the  misleading 


RESULTS  OF  SYPHILITIC  LESIONS          81 

postural  images  and  the  mental  state  has  deteriorated 
beyond  the  ataxic  threshold,  the  tabetic  feels  an  extraor- 
dinary effort  is  needed  to  move,  but  the  amount  of  that 
effort  he  has  no  means  of  gauging.  He  overestimates 
it.  For  simple  movements,  he  exerts  maximal  efforts. 
Maximal  efforts  not  merely  fatigue  him,  they  also  lead 
to  a  sacrifice  of  accuracy  in  direction  and  in  extent.  His 
endeavors  visually  to  guide  the  clumsy  movement  make 
it  still  more  clumsy.  With  exaggerated  force  he  starts 
to  move.  The  limb  jerks  forward,  at  first,  in  the  desired 
direction,  but  its  momentum  carries  it  onward  in  false 
paths.  He  sees  his  error,  arrests  the  movement;  over- 
corrects  the  error ;  stops  again ;  jerks  onward  once  more ; 
and  so4  by  a  zigzag  course  reaches  his  object  only  to  over- 
shoot it.  His  movement  thus  errs  mainly  through  his 
imperfect  conscious  control  of  it,  mainly,  therefore,  in 
its  spatial  qualities. 

In  extreme  cases  the  effort  needed  to  initiate  move- 
ment may  be  more  than  the  tabetic  can  command;  in 
spite  of  his  wish  to  move,  he  remains  stationary.  Or  if 
he  manages  to  make  the  effort  the  slightest  additional 
demand  upon  his  capacity  proves  "a  last  straw";  a 
crack  in  the  floor,  a  change  of  level,  encountered  while 
he  is  moving  brings  his  movement  to  a  humiliating  end. 

I  well  remember  my  chagrin  when  a  tabetic,  whom  I 
brought  before  my  class  in  the  Post-Graduate  Medical 
School,  in  June,  1913,  to  demonstrate  the  cure  of  his 
ataxia,  and  who  unaided  could  walk  excellently,  blind- 
folded, began  his  effort  before  the  class  by  punctiliously 
arranging  his  surroundings,  moving  a  chair  and  lifting  a 
tiny  piece  of  paper  from  the  floor,  by  adjusting  his 
garments,  by  rubbing  his  moist  hands,  and  by  ceremoni- 
ously preparing  himself  for  a  great  endeavor.  After 


82  LOCOMOTOR  ATAXIA 

two  or  three  sudden  steps  he  collapsed  in  a  heap  opposite 
an  imperceptible  crack  in  the  floor.  Then,  asked  to 
stand,  he  swayed  and  fell,  or  collapsed  without  swaying. 
Supported  by  my  little  finger,  which  he  rigidly  clutched, 
he  circled  freely  round  the  amphitheater.  The  aid  ren- 
dered him  was  altogether  disproportionate  to  its  effect. 
Another  tabetic,  at  present  under  my  care  at  the  Neuro- 
logical Hospital,  Blackwell's  Island,  refuses  to  walk; 
and  when  coerced  he  shuffles  slowly  and  extremely  cau- 
tiously along,  supporting  himself  on  both  sides  by  aid 
of  the  wall,  the  bedstead,  chairs  or  table ;  and  collapsing 
or  threatening  to  collapse  at  frequent  intervals. 

After  the  effort  of  starting,  the  tabetic  feels  to  some 
extent  that  not  he  but  "It"  moves.  All  tabetics  have 
difficulty  in  arresting  movement;  they  overshoot  their 
mark:  and  if,  while  walking,  they  are  suddenly  ordered 
to  halt,  they  fall  or  sway  widely.  In  Dejerine's  service 
in  the  Salpetriere,  in  1906,  I  saw  a  tabetic  who  was 
projected  into  a  run  by  the  effort  needed  to  start  move- 
ment and  who  could  stop  only  by  grace  of  an  obstacle. 

Every  influence  which  conduces  to  fatigue,  depression 
or  fear  conduces  to  ataxia;  every  influence  which  rests, 
reassures  and  cheers,  alleviates  ataxia.  Unfavorable 
mental  states  beget  ataxia  and  ataxia  engenders  un- 
favorable mental  states.  Tabetics  are  ataxic  because 
they  are  tired,  afraid,  and  depressed  and  tabetics  are 
tired,  afraid,  and  depressed  because  they  are  ataxic. 
The  ataxic  tabetic  reflects  his  fatigue  and  freshness,  fear 
and  courage,  cheerfulness  and  depression,  joy,  sorrow, 
excitement,  placidity,  anger,  pleasure  and  other  psychic 
states  by  alterations  in  the  degree  of  ataxia ;  ataxia  be- 
comes his  most  eloquent  mode  of  expression.  The  les- 
sening of  ataxia  during  favorable  mental  states,  such  as 


83 

freshness,  cheerfulness  and  calmness;  and  the  increase 
of  ataxia  during  unfavorable  mental  states  are  merely 
phenomena  of  these  mental  states. 

Without  the  conscious  sensory  defect  of  tabes,  there 
would  be  no  uncertainty;  no  suppression  of  the  critical 
after-images  of  posture;  no  clumsy  attempts  to  direct 
movement  by  vision;  no  meticulous  care;  no  dispropor- 
tionate effort ;  no  extravagant  movement ;  and  perplexity, 
anxiety,  fear  and  fatigue  would  not  disintegrate  the  men- 
tal capacity  of  the  tabetic,  would  not  create  in  him  motor 
tendencies  antagonistic  to  voluntary  control  of  move- 
ment. Without  the  reflex  defect  this  loss  of  voluntary 
control  would  not  result  in  ataxia.  So  long  as  desire  to 
maintain  or  to  assume  a  posture  can  excite  postural 
images  with  sufficient  intensity  to  compensate  for  the 
existing  reflex  defects,  the  tabetic  moves  coordinately. 
The  disturbance  revealed  in  the  tabetic's  attitude  and 
movement  is  mainly  a  measure,  not  of  the  structural 
defeats  in  the  reflex  mechanism  resulting  from  the  syph- 
ilitic invasion,  but  of  the  failure  of  conscious  control  of 
movement  to  compensate  for  these  defects. 

Deterioration  of  movement  in  the  tabetic  may  not  stop 
at  ataxia  but  may  pass  into  what  is  erroneously  called 
paralysis.  There  is  no  paralytic  stage  in  tabes.  An 
occasional  case  shows  extreme  muscular  atrophy  due  to 
syphilitic  implications  of  the  motor  neuron,  implications 
which  are  accidental  and  not  inherent  to  tabes.  Most 
of  the  muscular  wasting  of  tabes  is  not  a  paralytic,  but 
a  disuse,  atrophy.  Over  90  per  cent  of  the  so-called 
paralytic  cases  are  merely  cases  which  have  surrendered 
the  privilege  of  moving  rather  than  endure  the  tax  which 
movement  entails.  Some  resign  themselves  to  bed  life 
because  with  advancing  years  their  capacity  for  effort 


81  LOCOMOTOR  ATAXIA 

fails,  some  because  of  despair  following  failure  to 
obtain  relief  through  treatment;  but  most  because  they 
will  not  contend  against  arthropathies  and  ataxia,  or 
fractures  and  ataxia.  Some  indeed  become  bed-ridden 
who  were  never  ataxic  (see  p.  162).  I  have  seen 
several  in  whom  this  surrender  stage  ensued  within 
a  few  months  of  the  onset  of  ataxia.  They  were  remark- 
able in  showing  also  an  abnormally  short  preataxic  stage. 
The  mental  inferiority  which  conduced  to  the  short  pre- 
ataxic period  conduced  also  to  the  rapid  surrender  of 
all  voluntary  movement.  Indeed,  one  explained  she  had 
taken  to  bed  immediately  ataxia  developed  in  conse- 
quence of  the  death  of  her  daughter. 

The  bed-ridden,  as  a  rule,  do  not  remain  so.  Even 
without  treatment,  if  they  do  not  develop  bedsores,  they 
sooner  or  later  make  tentative  efforts  to  move  again 
and  oscillate  between  inactivity  and  action  according  to 
the  encouragement  to  effort  they  receive.  With  treat- 
ment all  can  be  made  to  rise  and  walk.  The  main  differ- 
ence between  the  ataxic  and  the  paralytic  stage  is  that 
in  the  ataxic  stage  the  tabetic  still  strives,  in  the  paralytic 
he  has  surrendered.  The  courageous  never  become  bed- 
ridden. Only  the  old  and  the  timid  seek  the  shelter  of  an 
effortless  existence. 

The  three  stages  of  degradation  of  voluntary  move- 
ment in  tabes  are  not  stages  of  structural  demolition 
but  stages  of  mental  deterioration.  The  first  or  pre- 
ataxic stage  is  the  stage  in  which  the  capacity  for  effort 
gradually  diminishes  until  the  ability  longer  to  mask 
the  spinal  lesions  by  increased  supervision  of  movement 
fails;  the  second  or  ataxic  stage  is  the  stage  in  which 
the  effects  of  the'  lesions  are  no  longer  masked  but  the 
desire  to  persist  active  incites  the  tabetic  to  move  in 


RESULTS  OF  SYPHILITIC  LESIONS          85 

spite  of  the  effort  movement  entails;  the  third  or  para- 
lytic stage  is  the  stage  in  which  the  desire  is  inadequate 
to  encourage  the  tabetic  to  the  effort  necessary  to 
movement. 


CHAPTER  V 

RESULTS    OF    THE    SYPHILITIC    INVASION    OF    CRANIAL 

NERVES 

The  olfactory  nerve.  The  optic  nerve.  Onset,  course  and  nature  of 
optic  atrophy.  Ophthalmoscopic  findings.  Psychic  and  struc- 
tural factors  in  visual  loss.  Effect  of  mescalin  in  enhancing 
vision.  Difficulty  of  measuring  visual  acuity.  Measurement  of 
light  perception  in  nearly  blind  tabetics.  Threshold  of  percep- 
tion of  light,  threshold  of  perception  of  change.  Blindness;  fre- 
quency, time  of  onset,  rate  of  development.  Causes  of  sponta- 
neous improvement  in  visual  acuity.  Absence  of  proof  that  optic 
tabes  arrests  spinal  tabes.  Influence  of  blindness  upon  ataxis. 
Spontaneous  cure  of  ataxia  following  blindness.  Influence  of 
blindness  upon  the  mental  state  and  upon  sensory  perception. 
The  relation  of  loss  of  vision  to  coordination.  Effect  of  blind- 
ness upon  pain  and  deafness.  Third,  fourth,  and  sixth  nerves. 
Diplopia,  its  causes;  squint;  spontaneous  cure.  Means  for  as- 
certaining the  presence  of  suppressed  visual  images.  The  fifth 
nerve.  The  seventh  nerve.  The  eighth  nerve.  Vestibular  le- 
sions. Auditory  mechanism.  Psychic  deafness.  Tabetic  deaf- 
ness. Influence  of  deafness  upon  the  mental  state.  Increase  of 
deafness  with  stationary  lesions.  Other  cranial  nerves. 

THE  syphilitic  invasion  called  tabes,  although  mainly 
concentrated  upon  the  posterior  nerve  roots,  may  begin 
in,  or  spread  to,  other  sites,  such  as  the  cranial  nerves. 
The  cranial  nerves  may  be  attacked  either  at  their 
nuclei  of  origin,  or  in  their  course.  The  nature  of  the 
attack  is  similar  to  that  described  as  occurring  in  the 
processes  of  the  posterior  root  fiber:  but,  owing  to  the 
long  intracerebral  course  of  many  of  the  cranial  nerves, 
they  tend,  perhaps  more  than  posterior  roots,  to  become 
involved  in  adventitious  patches  of  syphilitic  meningitis 
which  they  accidentally  encounter. 

86 


SYPHILITIC  CEANIAL  NERVES  87 

Among  the  cranial  nerves  the  olfactory,  or  first  nerve, 
is  not  rarely  affected.  The  resulting  loss  of  smell  is 
usually  bilateral. 

When  the  second,  or  optic,  nerve  is  implicated,  the 
attack  usually  occurs  early  in  the  disease.  When  tabes 
has  lasted  several  years  without  optic  atrophy,  optic 
atrophy  seldom  supervenes  (Pierre  Marie). 

Rarely  only  one  nerve  is  attacked.  Usually  the  spiro- 
chete  invasion  begins  in  one  nerve,  at  a  single  or  at 
several  points;  advances  for  a  time;  then  halts  there; 
and  recommences,  not  in  posterior  roots  or  elsewhere, 
but  in  the  other  optic  nerve.  The  destruction  of  the 
optic  nerve  may  stop  at  any  stage.  Complete  degenera- 
tion is  rare :  even  in  the  most  severe  cases  some  fibers 
almost  invariably  remain  unaffected.  The  invasion  may 
cause  only  slight  destruction.  When  the  optic  nerve  is 
the  first  site  attacked,  the  degeneration  usually  is  more 
complete  than  when  the  optic  follow  spinal  lesions. 

Just  as  in  the  posterior  root,  so  in  the  optic  nerve, 
the  invasion  is  essentially  primary;  the  lesions  are  not 
due  to  changes  either  in  the  nerve  cells  or  in  the  me- 
ninges.  Stargardt  found  not  the  retinal  cells  but  the 
intracranial  portion  of  the  optic  nerve  mainly  affected; 
sometimes  lesions  occurred  in  the  nerve  without  any 
detectable  change  in  the  retinal  cells;  and  the  changes 
in  the  nerve  were  always  more  extensive  than  in  the 
retina.  The  lesions  in  the  optic  nerve  also  bore  no  con- 
stant ratio  to  the  meningeal  changes  in  site  or  in  severity. 

Through  the  ophthalmoscope  the  affected  nerve  is  seen 
as  a  gray  disc  with  a  clearly  defined,  pigmented,  flat 
rim.  The  grayness  begins  on  the  temporal  side.  The 
fundal  vessels  shrink.  Gradually  the  whole  disc  may 
become  ivory  white,  with  here  and  there  atrophic  re- 


88  LOCOMOTOR  ATAXIA 

mains  of  blood  vessels.  This  pallor  may  rarely  be 
unilateral,  and  is  often  more  marked  in  one  eye  than 
in  the  other.  Accompanying  the  pallor,  contraction  of 
the  field  and  diminution  of  the  acuity  of  vision  occur. 
As  the  disease  affects  mainly  the  intracranial  portion 
of  the  nerve,  an  astonishingly  normal  looking  disc  may 
be  associated  with  considerable  loss  of  vision. 

Diminution  of  vision  begins  usually  in  one  eye, 
progresses  to  a  certain  point,  remains  stationary  there, 
and  then  commences  in  the  other  eye.  All  degrees  of 
loss  may  be  experienced  in  either  or  in  both  eyes.  The 
loss  of  vision  may  be  insignificant;  or  it  may  be  such 
that  scarcely  form  can  be  detected.  Vision,  in  severe 
cases,  is  usually  lost  to  the  same  degree  in  both  eyes. 
As  the  perception  of  light  is  a  function  of  the  whole 
retina,  and  as  the  optic  nerve  is  practically  never  com- 
pletely destroyed,  the  blind  tabetic  can  almost  always 
distinguish  light  from  darkness.  The  reading  of  stan- 
dard type  is  usually  employed  to  test  for,  and  to  meas- 
ure, gross  changes  in  visual  acuity.  To  estimate  the 
contraction  of  the  visual  field,  we  use  the  perimeter. 
By  means  of  colored  wools,  loss  of  perception,  first  of 
green,  next  of  red,  and  then  of  blue  and  of  yellow,  may 
be  found  in  the  tabetic. 

By  subcutaneous  injection  of  mescalin  sulphate,  a  salt 
of  the  alkaloid  of  the  Mexican  drug,  pelotte,  the  mescal 
button  (Anhalonium  Lewinii),  Dr.  A.  Knauer  and  I 
produced,  in  ourselves  and  others,  an  intoxication  in 
which  attention  is  restricted  to  one  subject  at  a  time. 
Any  subject  while  under  consideration  by  the  intoxicated 
person  occupies  conscious  attention  in  a  much  more 
intense  and  exclusive  manner  than  normal. 

In  testing  with  this  drug  a  series  of  eight  blind  or 


SYPHILITIC  CRANIAL  NERVES  89 

nearly  blind  tabetics,  four  of  them  patients  of  Dr.  Wachs- 
mann,  the  distinguished  director  of  the  Montefiore  Home, 
one  a  patient  of  Dr.  Abrahamson,  and  three  patients  of 
mine  in  the  Neurological  Hospital,  I  obtained  astounding 
results.  Visual  fields  enlarged  enormously,  especially 
for  red  and  green.  Visual  acuity  as  measured  by  Snel- 
len's  type  increased  greatly;  indeed,  some  were  enabled 
to  read  who  before  injection  could  not.  One  tabetic,  R., 
who  could  distinguish  little  more  than  light  from  dark- 
ness, when  I  went  to  examine  him  half  an  hour  after 
injection,  was  tossing  coins  on  the  floor  and  stooping 
to  pick  them  up  without  groping.  He  spent  that  night 
in  a  fever  of  excitement,  dragging  his  friends  to  moving 
picture  shows  that  he  might,  by  describing  what  he  saw 
on  the  screen,  convince  them  of  the  miraculous  restora- 
tion of  his  sight.  He  passed  freely  through  traffic  and 
entered  and  left  vehicles  as  do  those  who  see.  The  effect 
persisted  for  five  days;  after  the  second  day  it  declined 
rapidly,  but  during  the  first  three  days  it  was  very  evi- 
dent. 

These  experiments  emphasize  how  dependent  we  are 
upon  what  the  patient  reveals  for  our  knowledge  of 
visual  defects,  and  also  how  we  may  form  false  conclu- 
sions, as  to  the  extent  of  the  optic  lesions,  from  what  the 
patient  imparts  to  us.  Hence,  it  is  not  astonishing  that 
grayness  may  be  present  in  the  optic  disc  and  the  vision 
remain,  apparently,  almost  normal. 

In  fifteen  tabetics  in  whom  only  a  trace  of  vision  per- 
sisted, I  tested  the  light  perception,  using  standardized 
electric  lamps  of  1,  2,  4,  6,  8,  16,  32,  and  64  candle  power. 
The  tabetic  was  seated  in  a  dark  room,  at  a  constant 
distance  from  the  source  of  light,  with  his  back  to  it, 
so  as  to  avoid  unequal  stimulation  of  any  part  of  the 


90  LOCOMOTOR  ATAXIA 

retina,  and  six  feet  from  it,  so  that  he  could  not  perceive 
the  heat  changes.  The  light  was  turned  on  and  off,  not 
by  means  of  the  switch,  but  noiselessly  by  turning  the 
bulb  in  the  socket.  Each  eye  was  tested  separately. 
The  patient  was  instructed  to  say  " Lighter,"  " Darker," 
' '  Same, "  "  Change, ' '  according  to  what  he  perceived  and, 
from  the  beginning  to  the  end  of  the  experiment,  to 
respond  without  being  questioned. 

A  change  in  illumination  was  sometimes  confidently 
and  correctly  announced  after  one  or  two  false  responses, 
the  perception  apparently  having  been  delayed.  When 
this  was  evident,  responses  were  required  at  intervals 
longer  than  this  latent  period.  The  tabetic  responded 
synchronously  with  every  beat  of  a  slow  moving  metro- 
nome. The  stimulus  was  changed  at  regularly  irregular 
intervals,  to  preclude  guessing.  In  order  that  answers 
based  on  false,  might  not  obscure  those  based  on  true, 
premises,  fifty  responses  were  required  in  each  test. 
The  proportion  of  correct  answers  given  by  the  same 
patient  to  the  same  stimulus  was  liable  to  vary  from 
day  to  day.  The  lowest  candle  power  which  on  three 
successive  days  yielded  not  less  than  fifty  per  cent  of 
correct  answers,  was  taken  as  the  visual  threshold. 

The  equalizing  of  the  retinal  stimulation,  the  elimina- 
tion of  heat  and  of  noise  from  the  light  changes,  the 
number  of  observations,  and  the  repetition  of  the  tests, 
made  the  threshold  thus  obtained  an  approximately  ac- 
curate index  of  the  tabetics  actual  perception  of  light. 

The  correctly  perceived  change  was  often  described  as 
a  sudden  flash  or  a  sudden  shadow,  sometimes  as  a 
movement  in  apparently  hallucinatory  lights  and  shades. 
A  change  was  sometimes  perceived,  and  its  nature  not. 
There  were,  therefore,  distinguishable  two  thresholds, 


SYPHILITIC  CRANIAL  NERVES  91 

that  of  perception  of  light,  and  that  of  change.  Delu- 
sions were  evident,  particularly  near  the  visual  thresh- 
old; and  there  fatigue  was  quickly  produced. 

Some  of  the  patients  who  could  tell  how  many  windows 
were  in  a  ward,  how  many  panes  in  a  window,  could 
describe  the  appearance  of  their  fellow  denizens,  and 
otherwise  offer  spurious  proof  of  vision,  had  thresholds 
of  32  or  64  candle  power  at  a  distance  six  feet  from 
the  source  of  light,  thresholds  which  precluded  any  ap- 
preciation of  form. 

In  periodical  examinations,  if  the  number  of  correct 
responses  progressively  diminishes,  the  conclusion  is 
inevitable  that  vision  is  deteriorating.  Sometimes  the 
first  sign  of  this  deterioration  was  the  rapidity  with 
which  fatigue  occurred;  accurate  results  were  then  ob- 
tained only  in  the  first  ten  or  twenty  responses.  After 
the  perception  of  light  was  lost,  the  ability  to  detect 
change  of  illumination  still  persisted.  In  one  case,  with 
a  32  candle  power  light  the  change  from  light  to  dark- 
ness was  not  perceived,  but  that  from  darkness  to  light 
almost  invariably  was. 

The  occurrence  of  blindness  in  tabes  was  observed 
first  by  Romberg  (1841-51).  The  great  Duchenne  in  his 
original  description  of  "ataxie  locomotrice  progressive" 
mentions  two  cases  associated  with  blindness.  Blind- 
ness was  thought  by  the  pioneer  investigator  to  be  a 
common  phenomenon  of  tabes.  Indeed,  Duchenne  found 
optic  atrophy  in  seventeen  out  of  twenty  tabetics. 

Von  Grosz  found  among  one  hundred  tabetics  disease 
of  varying  gravity  in  the  optic  discs  of  eighty-eight.  In 
this  total  he  includes  congestion,  tortuous  veins,  changes 
in  the  color  of  the  disc,  any  trace  of  departure  from  his 
normal  standard.  He  does  not  with  these  findings  give 


92  LOCOMOTOR  ATAXIA 

statistics  of  his  observations  of  similarly  trivial  abnor- 
malities in  the  optic  disc  of  average  non-syphilitic  in- 
dividuals of  the  same  age  as  the  tabetics  he  examined. 
K.  Mendel  and  Tobias  found  thirty-six  cases  (8.3  per 
cent)  of  severe  optic  atrophy  in  four  hundred  and  thirty 
cases  of  tabes  at  all  stages.  E.  Mendel  noted  twenty-one 
cases  (7.3  per  cent)  of  blindness  in  two  hundred  and 
eighty-eight  tabetics.  These  figures  conclusively  prove 
that  if  syphilis  attacks  the  optic  nerve  fibers  oftener 
than  we  suspect,  in  the  vast  majority  of  cases  neither 
blindness  nor  even  a  severe  degree  of  atrophy  results. 

In  Martin's  twenty-one  cases  of  blindness,  the  blind- 
ness followed  the  ataxia  only  once ;  in  Leri's  forty,  thrice ; 
in  Schiipfer's  twenty-four,  once:  in  these  eighty-five 
blind  tabetics,  blindness  followed  ataxia  only  five  times 
(5.9  per  cent).  Syphilitic  atrophy  beginning  in  the  optic 
nerve,  therefore,  much  oftener  leads  to  blindness  than 
atrophy  affecting  the  optic  nerve  after  other  sites  have 
been  attacked. 

Among  Elschnig's  forty  cases  of  tabetic  blindness, 
thirty-one  became  blind  within  two  years  of  the  first 
symptom  of  affection  of  the  optic  nerve.  Of  these  thirty- 
one,  thirteen  became  blind  in  three  months;  five,  in 
six;  nine,  in  twelve;  and  four  in  twenty-four. 

Blindness  often  occurs  more  speedily.  Indeed,  among 
neurological  traditions  is  one  of  a  tabetic  on  board  a 
ship  in  the  tropics  who  with  his  fellow  passengers  was 
timing  the  sunset :  while  the  sun  was  still  on  the  horizon 
he  exclaimed,  "It's  gone."  Blindness  had  suddenly 
struck  him.  An  engineer,  aged  thirty-six,  went  to  bed, 
in  apparently  normal  health,  and  in  the  darkness  of  a 
winter  morning,  thinking  it  was  his  usual  time  to  rise, 


SYPHILITIC  CRANIAL  NERVES  93 

s track  a  match  to  enable  him  to  see  his  watch.  To  his 
astonishment,  although  no  flame  was  visible,  he  burnt 
his  fingers.  He  came  to  the  National  Hospital,  London, 
where  I  was,  at  the  time,  House  Physician.  He  seemed 
quite  blind:  he  had  bilateral  optic  atrophy:  there  was 
a  probable  decrease  in  his  knee-jerks  and  he  had  incon- 
trovertible loss  of  sensibility  to  pain  (pinprick)  over 
root  areas  in  the  lower  limbs.  Sudden  blindness  is  a 
highly  improbable  consequence  of  mere  structural  change 
in  the  optic  nerves,  and  resembles  more  a  paretic  than 
a  tabetic  phenomenon. 

Syphilitic  degeneration  of  the  optic  nerve  fibers  is 
irreparable.  The  visual  loss  once  established  is,  as  a 
rule,  permanent.  But  Gowers  and  others  have  recorded 
cases  of  improvement  of  measurable  extent.  The  par- 
tial destruction  of  some  of  many  paths  conveying  im- 
pulses concerned  in  the  same  function,  at  first,  especially 
if  the  destruction  occur  rapidly,  may  derange  the  whole 
function.  Soon  this  excessive  impairment  passes  off  and 
the  true  degree  of  disturbance  of  vision  alone  remains. 
One  of  my  patients,  whose  blindness  developed  rapidly 
until  the  visual  threshold  for  light  perception  was  higher 
than  a  thirty-two  candle  power  light,  at  a  distance  of  six 
feet,  without  treatment,  subsequently  perceived  correctly 
nearly  every  change  in  illumination  with  a  four  candle 
power  lamp.  Moreover,  with  the  onset  of  loss  of  vision, 
such  profound  depression  and  mental  perturbation  result 
that  the  confessed  is  seldom  a  true  index  to  the  real 
visual  acuity.  Spontaneous  improvement  in  vision  may 
be  due  to  three  factors;  first,  to  the  absorption  of  an 
accompanying  meningeal  or  interstitial  exudate  which 
by  pressure  on  the  optic  nerves  is  impeding  their  func- 


94  LOCOMOTOR  ATAXIA 

tion;  second,  to  the  readjustment  of  the  visual  faculty 
to  the  structural  defect ;  and  third,  to  the  recovery  from 
unfavorable  mental  states.  Much  of  the  alleged  remedial 
effect  of  mercury  and  of  salvarsan  is  attributable  to  the 
last  two  of  these  factors.  I  have  never  been  able,  by  the 
methods  of  examination  I  have  described,  to  detect  any 
benefit  from  the  administration  of  these  substances. 

In  1881,  Moriz  Benedikt  of  Vienna  asserted  that  tabes 
associated  with  rapid  optic  atrophy  shows  benign  spinal 
symptoms.1 

He  grew  in  optimism.  In  1887,2  in  an  open  letter  to 
Babinski  in  the  Wiener  medicinische  Wochenschrift,  he 
emphasized  his  insinuation  of  1881.  He  proclaimed  a 
law  to  which  till  then  he  knew  no  exception,  that  the 
specific  motor  symptoms  of  tabes,  no  matter  to  what 
degree  they  had  attained,  would  diminish  in  severity  im- 

1  "Obwohl  wir  nicht  irn  Stande  sind  auf  dem  Verlauf  der  Sehner- 
venatrophie  irgend  einen  wesentlichen  Einfluss  zu  nehmen  dieselbe 
vielmehr  gewohnlich  rapid  usque  ad  ultimum  f ortschreitet  so  kb'nnen 
wii  doch  im  Bezug  auf  die  spinalen  Symptomen  wenn  sie  noch  so 
ausgebildet  und  intensiv  sind  die  Prognose  hochst  gunstig  stellen.  Eine 
Ausnahme  machen  vielleicht  nur  sehr  veraltete  Falle.  Es  kann  gesche- 
hen  dass  mit  Ausnahme  des  Schwankens  beim  Stehen  mit  geschlossenen 
Augen  und  der  Sehnen  reflexe  die  nicht  mehr  zum  Yorscheine  komnien 
alle  ataktischen  Symptomen  schwinden." 

*  "Ueber  die  Prognose  und  Therapie  der  Tabes."  Offener  Brief  an 
Herrn  Dr.  T.  Babinski  in  Paris,  Wiener  med.  Wochenschrift,  Aug.  14, 
1887,  p.  1130. 

"Es  ist  ein  Gesetz  von  dem  ich  personlich  bis  jetzt  absolut  keine  Aus- 
nahme kenne,  dass  die  specifischen,  tabetischen  motorischen  Erschein- 
ungen  wenn  sie  einen  noch  so  hohen  Grad  erreicht  haben,  zuriick  gehen, 
sobald  die  Krankheit  mit  Sehnervenatrophie  eingesetzt  hat." 

"Ich  babe  seit  dem  z.  B.  einen  Fall  (Case  399)  mit  prodromaler 
Sehnervenatrophie  beobachtet  der  absolut  nicht  mehr  im  Stande  war 
zu  stehen  und  einen  Schritt  zu  gehen,  der  aber  unter  entsprechender 
Behandlung  so  hergestellt  wurde  das  er  jahrelang  obwohl  total  er- 
blindet  die  compliciersten  Gange  in  der  Stadt  machte." 


SYPHILITIC  CRANIAL  NERVES  95 

mediately  the  disease  became  complicated  by  atrophy  of 
the  optic  nerve. 

Dejerine  and  Martin,1  in  1889,  from  studying  one  hun- 
dred cases  of  tabes,  eighteen  of  which  showed  optic 
atrophy,  concluded  that  optic  atrophy  occurring  at  the 
beginning  of  tabes  arrests  almost  always  the  develop- 
ment of  sclerosis  of  the  posterior  columns,  and  at  the 
same  time  diminishes  the  sensory  symptoms.  So  far, 
they  state,  "la  proposition  de  Benedikt  est  exacte."  But 
they  believed  they  had  demonstrated  that  once  the  inco- 
ordination  is  established,  blindness  does  not  influence 
the  further  course  of  the  disease.2  Martin,  in  his  thesis 
published  the  following  year,  dealt  with  twenty-one  cases 
of  tabetic  optic  atrophy  and  reiterated  the  views  he  had 
already  expressed  with  his  master.  Raymond  tends  to 
agree  with  Dejerine  and  Martin.  Ingelrans  in  1897 
supported  Benedikt 's  "law"  in  its  entirety.  So  did 
Forster  in  1900;  and  to  a  greater  or  less  extent  so  also 
did  Benenati  in  1901,  and  Schiipfer  in  1901. 

Buzzard,  Leri  and  others  have  opposed  the  law. 

Ataxia  is  an  inaccurate  guide  to  the  extent  of  the 
spinal  lesions,  yet  it  has  been  used  by  those  who  opposed 
and  those  who  upheld  the  idea  that  optic  tabes  benignly 
influences  spinal  tabes.  The  cases  published  in  this  dis- 
cussion show  ataxia  may  follow  optic  atrophy ;  and  optic 
atrophy  may  follow  ataxia.  Optic  tabes,  therefore,  does 
not  preclude  spinal  tabes  nor  does  spinal  tabes  preclude 
optic.  They  further  show  that  ataxia  usually  does  not 

1  "L'atrophie  papillaire  survenant  au  debut  du  tabes  arrete  presque 
toujours  revolution  de  la  sclerose  des  cordons   posterieurs  en  meme 
temps  qu'elle  diminue  les  symptomes  d'ordre  sensitifs." 

2  "Lorsque  1'incob'rdination  est  etablie  la  cecite  n'influe  en  rien  sur  la 
marehe  de  cette  derniere." 


96  LOCOMOTOR  ATAXIA 

follow  optic  atrophy  nor  does  optic  atrophy  usually  fol- 
low ataxia ;  and  that  tabetics  with  optic  atrophy  have 
more  seldom  spinal  lesions  than  have  those  without  optic 
atrophy. 

There  is  in  this  evidence  no  proof  of  any  arrest  of 
optic  atrophy  by  spinal  tabes  nor  of  spinal  tabes  by  optic 
atrophy ;  but  there  is  proof  that  the  chief  stress  of  optic 
tabes  falls  upon  the  optic  nerve  and  not  upon  the  spinal 
mechanism;  and  that  the  chief  stress  of  spinal  tabes 
falls  upon  the  spinal  mechanism  and  not  upon  the  optic. 
There  is  also  proof  that  tabes  beginning  in  the  optic 
nerve  is  often  limited  mainly  to  it. 

If  there  is  a  causal  relation  between  optic  atrophy  or 
blindness,  and  the  retention  of  the  power  of  coordination, 
then  this  relationship  should  be  most  evident  when  the 
optic  atrophy  reduces  vision  to  a  degree  which  precludes 
all  the  aid  to  movement  normally  derived  from  sight. 

Indisputably,  blind  tabetics  are  less  prone  to  ataxia 
than  seeing  tabetics.  From  comparing  blind  with  seeing 
tabetics,  we  can  reach  no  conclusion  as  to  the  existence 
of  any  influence  of  blindness  upon  ataxia,  unless  the 
contrasted  blind  and  seeing  possess  equally  extensive 
incoordinating  lesions.  To  demonstrate  the  precise  ex- 
tent of  the  incoordinating  lesions  is  difficult.  If  series 
of  blind  and  seeing  tabetics  with  equally  extensive  lesions 
were  collected  and  examined,  the  ataxia  might  be  found 
to  vary  among  the  seeing  just  as  much  as  between  the 
average  seeing  and  the  average  blind  ataxic.  The  only 
conclusive  evidence  of  the  influence  of  blindness  upon 
ataxia  is  obtainable  by  clinical  observation  of  the  effect 
of  blindness  supervening  upon  ataxia.  When  in  ataxic 
cases  blindness  supervenes,  no  question  of  the  extent  to 
which  the  tabetic  lesions  affect  the  cord  can  arise,  for 


97 

before  the  onset  of  the  blindness  the  lesions  were  such 
that  ataxia  had  already  arisen.  The  cord  lesions  were 
present,  the  ataxia  existed,  blindness  supervened,  what 
was  the  result? 

Benedikt,  in  1887,  stated,  and  I  cannot  find  that  he 
subsequently  modified  his  statements,  that  he  had  never 
yet  seen  a  case  in  which  improvement  in  spinal  symp- 
toms did  not  occur.  His  statement  implied  that  he  had 
seen  cases  in  which  improvement  did  occur.  I  have 
searched  his  publications  and  found  only  one  case.  He 
makes  such  use  of  this  single  case  that  if  he  had  had 
others,  he  would  have  been  likely  to  disclose  them.  Mar- 
tin (1890)  reports  one  case  of  marked  improvement  in 
ataxia  when  complete  optic  atrophy  occurred,  but  he 
remarks  that  remissions  in  tabes  are  frequent,  and  that 
this  isolated  example  does  not  suffice  to  establish  a 
causal  relationship  between  the  blindness  and  the  dis- 
appearance of  the  ataxia.  He  was  dealing  with  a  blind 
tabetic ;  any  example,  however  isolated,  of  such  a  strange 
phenomenon  as  permanent  remission  of  ataxia  associated 
with  blindness,  demands  explanation. 

Bouchaud  records  a  case  in  which,  between  1875  and 
1882,  there  were  among  other  symptoms  much  motor 
trouble,  disordered  movements  of  the  lower  limbs,  and 
some  incoordination  of  the  upper  limbs.  In  1882,  the 
vision  began  to  fail :  by  1884,  blindness  was  absolute,  but 
the  symptom,  ataxia,  had  ameliorated :  in  1891,  the  inco- 
ordination had  disappeared:  not  even  Komberg's  sign  re- 
mained. 

Inglerans  records  two  tabetic  women  in  Dejerine's 
service  who  were  definitely  ataxic  and  whose  ataxia  dis- 
appeared when  they  became  blind.  Madame  A.  (Obser- 
vation xxix)  became  ataxic  in  1882,  and  blind  in  1884; 


98  LOCOMOTOR  ATAXIA 

her  ataxia  subsequently  disappeared;  in  1897  she  still 
walked  correctly.  Madame  Del.  (Observation  xxxvi) 
was  ataxic  from  1885,  and  developed  blindness  in  1889; 
soon  after,  the  ataxia  began  to  disappear;  in  1897,  she 
had  no  signs  of  motor  incoordination. 

Forster  describes  two  cases  of  ataxia  (cases  15  and  19) 
in  which  so  great  improvement  followed  the  onset  of 
blindness  that  the  disease  returned  to  the  preataxic  stage. 
In  one,  incoordination  was  evident  only  in  running;  in 
the  other,  only  in  the  dark. 

Benenati  (1901)  reports  two  cases  of  ataxia  amelio- 
rated by  the  onset  of  optic  atrophy.  The  first,  a  man,  had 
normal  vision  in  the  right  eye.  The  improvement  in 
the  ataxia  Benenati  attributes  to  the  complete  optic 
atrophy  in  the  left  eye.  This  case  certainly  should  not 
be  held  to  prove  anything.  Loss  of  one  eye  in  normal 
life  does  not  influence  equilibrium.  The  other  case,  a 
woman,  had  gray  atrophy,  but  all  the  information  given 
is,  "La  vista  e  molto  ridotta  in  ambo  gli  occhi." 

Schiipfer  (1901)  reports  five  cases  of  improvement  in 
ataxia  following  the  onset  of  optic  atrophy  (cases  2,  5, 
11,  23,  24).  Case  5  he  disallows  because  he  thinks  the 
disturbance  of  locomotion  was  due  to  the  onset  of  blind- 
ness. But  when  these  disturbances  appeared,  the  patient 
had  still  one-tenth  vision  in  both  eyes.  One-tenth  vision 
enables  form  to  be  distinguished  and,  therefore,  is  not 
an  adequate  explanation  of  "disturbi  dell'equilibrio " 
(p.  253).  Three  years  later,  " deambulazione  ottima, 
assenza  di  atassi"  (p.  254)  is  reported. 

I  am  indebted  to  Dr.  Isador  Abrahamson,  neurologist 
to  the  Montefiore  Home,  New  York  City,  for  the  follow- 
ing interesting  example :  Max  Krasnow,  in  1906,  at  the 
age  of  40,  was  attacked  with  lightning  pains  followed 


SYPHILITIC  CRANIAL  NERVES 


99 


by  numbness  of  the  right  leg.  Six  months  later  vision 
began  to  fail,  first  in  the  left  eye,  then  in  the  right.  In 
the  year  1906-07,  ataxia  appeared.  As  vision  deteri- 
orated, the  ataxia  increased.  About  the  beginning  of 
1908  he  became 
totally  blind.  He 
entered  the 
Montefiore  Home 
on  April  24,  1908. 
His  gait  then  was 
wildly  ataxic.  He 
began  spontane- 
ously to  walk  bet- 
ter and  continued 
to  improve  till  his 
ataxia  disappear- 
ed. He  now  is  so 
steady  that  he 
acts  as  a  prop 
and  a  guide  for 
other  ataxic  pa- 
tients (Fig.  42). 


FIG.  42. — Dr.  Abrahamson's  case.  Max  Krasnow 
(on  the  reader's  right)  while  able  to  see  was 
very  ataxic.  Since  he  became  blind  his 
ataxia  has  disappeared  and  his  attitude  has 
become  normal  again.  He  is  here  shown  aiding 
a  seeing  ataxic  to  walk. 


Leri  reluctant- 
ly admits  one  case 
(Harr,  p.  115). 
Harr  was  very 
ataxic  from  1888-1890 ;  in  1889,  while  under  observation 
in  Bicetre,  his  blindness  developed:  according  to  Leri, 
Harr  now  (1903)  walks  more  as  a  blind  man  than  as 
an  ataxic. 

I  have  demonstrated  three  cases,  one  of  which  is  now 
in  the  Neurological  Hospital,  to  the  Students  at  Fordham 
University  and  at  the  New  York  Post-Graduate  Medical 


100  LOCOMOTOR  ATAXIA 

School.  But  only  in  one  of  them,  Rose,  did  improvement 
occur  under  my  observation.  The  others  gave  a  history 
of  ataxia,  but  could  all  stand  and  walk  coordinately  when 
I  first  saw  them.  The  ataxia  in  Rose  was  slight;  he 
now  shows  no  trace  either  of  ataxia  or  of  swaying. 

Leri  objects  to  accepting  the  word  of  the  patient  re- 
garding the  degree  of  ataxia  before  and  after  blindness. 
The  patient  is  the  best  judge  of  his  own  wralking  ability 
which  he  tends  so  little  to  exaggerate  that  Leri's  objec- 
tion to  this  evidence  seems  scarcely  justified.  If  all 
cases  in  which  the  improvement  in  ataxia  did  not  occur 
under  medical  supervision  be  excluded,  the  exclusion 
affects  Martin's  case,  and  one  at  least  of  Schiipfer's,  and 
the  two  I  have  demonstrated.  Both  of  Benenati's  should 
be  eliminated,  because  in  neither  did  blindness  exist. 

Cases  have  been  reported  of  ataxia  disappearing  after 
the  onset  of  blindness  in  which  some  remedial  measure, 
such  as  hot  baths,  galvanism,  etc.,  was  alleged  to  have 
induced  the  improvement.  These,  which  I  have  not 
quoted,  include  Benedikt's  solitary  case,  for  that  patient 
at  some  time  subsequent  to  his  blindness  received  much 
electrical  treatment,  to  which  Benedikt  attributes  some 
of  the  credit  for  the  lack  of  ataxia. 

There  now  remain  as  indubitable  cases  in  which  im- 
provement of  ataxia  occurred  spontaneously  after  the 
onset  of  blindness,  Bouchaud's  case,  Leri's  case,  Abra- 
hamson's  case,  two  of  Inglerans',  two  of  Forster's,  three 
of  Schiipfer's,  and  one  of  mine,  a  total  of  eleven. 

The  claim  that  ataxia  may  spontaneously  decrease  in 
blindness  rests,  so  far  as  I  know,  only  upon  these  eleven 
cases.  One  incontestable  case  would  suffice  to  prove  the 
fact.  But  the  cumulative  effect  of  eleven  incontrovertible 
cases  has  a  corroborative  value  far  exceeding  that  which 


SYPHILITIC  CRANIAL  NERVES  101 

estimate  by  arithmetical  or  even  geometrical  progression 
would  confer.  These  eleven  cases  establish  absolutely 
that  in  blindness  coordination  may  spontaneously  in- 
crease, ataxia  may  spontaneously  decrease.  Blindness, 
we  have  seen,  affects  not  more  than  eight  per  cent  of 
tabetics,  probably  less;  and  blindness  follows  ataxia  in 
about  six  per  cent.  If  blindness  follows  ataxia  in  six 
per  cent  of  the  syphilitic  blind,  and  not  more  than  eight 
per  cent  of  tabetics  are  blind,  the  possibility  of  observing 
the  effect  of  blindness  upon  ataxia  occurs  in  not  more 
than  0.48  per  cent  of  tabetics.  But  Mott  claims  that 
50  per  cent  of  optic  atrophies  subsequently  develop  gen- 
eral paresis ;  so  the  opportunity  to  observe  improvement 
may  occur  in  less  than  0.24  per  cent.  These  figures  do 
not  pretend  to  any  absolute  value;  they  are  stated  only 
to  show  that  the  scarcity  of  the  evidence  is  not  due  to 
the  exceptional  nature  of  the  fact  which  it  establishes 
but  to  the  rarity  of  cases  which  yield  incontrovertible 
proof  of  that  fact. 

Byrom  Bramwell  reports  a  case  of  a  tabetic  in  whom, 
after  two  years  of  blindness,  ataxia  appeared,  and  ad- 
vanced rapidly  till  the  patient  could  not  stand;  among 
others,  both  Martin  and  Leri  report  two  analogous  cases. 

Simultaneously  with  the  onset  of  blindness  ataxia  may 
develop.  Such  cases  have  been  observed  by  Pearce 
Bailey,  Schiipfer,  myself  and  others.  Or  if  the  ataxia 
is  already  established,  as  in  Abrahamson's  case,  it 
usually  first  becomes  aggravated  by  blindness. 

The  benign  influence  of  blindness  upon  ataxia  is, 
therefore,  neither  invariable  nor  inevitable,  nor  is  it 
immediate,  but  develops  some  time  after  vision  is  lost 
and  tends  to  increase  with  the  duration  of  the  blind- 
ness. 


102  LOCOMOTOE  ATAXIA 

As  long  as  an  ataxic  sees,  he  is  a  creature  at  the  mercy 
of  his  environment.  By  day  his  environment  is  chang- 
ing constantly;  he  is  ever  striving  to  keep  pace  with  it; 
ever  painfully  alert  and  watchful;  confronted  with  a 
fresh  problem  wherever  his  gaze  rests.  He  must  con- 
stantly fight  against  his  economic  disability.  He  is 
harassed,  perplexed  and  fearful.  He  doubts  and  dreads 
every  influence  he  does  not  see. 

The  blind  tabetic  lives  a  life  of  enforced  inaction;  he 
is  outside  all  social  strife ;  he  reacts  only  to  his  immediate 
surroundings,  to  the  simple  reflex  problems  which  pene- 
trate his  darkened  life.  He  sees  less;  therefore,  fears 
less,  worries  less,  thinks  less.  He  may  be  depressed  but 
he  is  less  fatigued  and  less  fearful  than  the  seeing 
tabetic.  His  mental  state,  therefore,  improves ;  his  capac- 
ity for  effort  and  for  attention  increases.  His  postural 
sense  claims  its  share  in  the  attention  bequeathed  by 
vision.  The  longer  the  blindness  lasts,  other  things  being 
equal,  the  more  the  mental  state  improves.  With  this 
improvement  the  psychic  influences  unfavorable  to 
coordinate  movement  diminish :  and  in  the  constant  calm 
in  which  the  blind  tabetic  exists,  necessity  and  lack  of 
distraction  confer  an  interest  upon  the  hitherto  despised 
and  suppressed  postural  images.  They  still  remain 
feeble,  few,  and  imperfect,  but  he  learns  to  appreciate 
them,  to  interpret  them,  to  discriminate  changes  among 
them.  As  he  gains  knowledge,  he  gains  confidence,  he 
gains  power  to  move. 

The  law  of  the  relation  of  loss  of  vision  to  ataxia, 
if  it  can  be  dignified  as  a  law,  should  be :  Ceteris  paribus, 
of  two  tabetics,  at  any  stage  of  the  disease,  one  blind, 
the  other  seeing,  the  blind  has  the  greater  tendency  to 
persist  coordinate,  the  lesser  tendency  to  become  ataxic. 


SYPHILITIC  CRANIAL  NERVES  103 

The  degree  of  this  compensatory  improvement  in  the 
power  of  coordination  will,  ceteris  paribus,  tend  to  rise 
with  the  duration  of  the  blindness  to  a  degree  depending 
upon  the  training  capacity  of  the  tabetic.  Slinger  and 
Horsley  observed  that  the  postural  sense  of  the  non- 
tabetic  blind  ending  a  course  of  training  was  one-fourth 
greater  than  that  of  those  beginning  their  training  (see 
p.  59).  The  amount  of  improvement  in  movement  which 
may  occur  spontaneously  in  blindness  is  usually  remark- 
able; and  may  be  such  that  no  discernible  sign  of  in- 
coordination  can  be  detected. 

In  Bouchaud's  case  the  ataxia  began  to  decrease  soon 
after  the  blindness  occurred  in  1884,  and  in  1891  not 
even  Romberg's  sign  was  present.  Inglerans'  observa- 
tions show  a  similar  improvement:  the  whilom  ataxic, 
Madame  A.,  still  walked  correctly  after  fifteen  years  of 
blindness,  and  Madame  Del.,  after  nine  years,  showed  no 
sign  of  reverting  to  incoordination.  Leri's  case,  Harr, 
did  not  lose  his  attaxia  till  he  had  been  one  year  blind; 
after  fourteen  years  he  continued  to  walk  more  as  a 
blind  man  than  as  an  ataxic.  Abrahamson's  case,  after 
a  temporary  aggravation  of  the  ataxia,  showed  gradual 
improvement,  till  at  the  end  of  six  years  there  was  no 
sign  of  ataxia. 

As  blind  tabetics  are  less  ataxic  because  they  are  blind, 
the  long  preataxic  stage  of  the  blind  is  not  solely  an 
accident  of  localization  of  the  tabetic  lesion  in  the  optic 
nerve,  but  is  due  in  part  to  the  tranquil  mental  state 
which  blindness  ensures.  In  other  words,  the  blind 
tabetic  tends  to  remain  preataxic  after  his  spinal  lesions 
have  passed  a  point  at  which  a  seeing  tabetic  would  have 
become  ataxic.  Dejerine,  Babinski,  and  others  have 


104  LOCOMOTOR  ATAXIA 

found  in  autopsies  upon  blind  tabetics  with  no  ataxia, 
astonishingly  widespread  spinal  lesions. 

The  relations  of  blindness  to  ataxia  may  be  postulated 
as  follows:— 

I.  Improvement  in  ataxia  will  result  from  blindness 
after  an  adequate  interval  has  elapsed : 

(a)  When  incoordinating  lesions  remain  station- 
ary, and  the  mental  capacity  for  training  is  not 
destroyed  by  cerebral  disease. 

(b)  Even  if  the  structural  tabetic  lesions  leading 
to  incoordination  extend,  provided  that  the  effect 
of  this  extension  be  less  than  the  compensating  influ- 
ence of  the  blindness  upon  the  mental  state. 

II.  No  change  in  the  ataxia  will  follow  loss  of  vision 
if  the  advance  of  the  incoordinating  lesion  just  neutral- 
izes the  beneficial  influence  of  the  blindness.    Obviously 
this  stationary  phase  can  be  but  temporary. 

III.  Increase    of   ataxia   in   spite    of   the   blindness 
arises : 

(a)  When    the    incoordinating    lesions    advance 
faster  than  the  coordinating  tendency  of  the  blind- 
ness grows.     Here  increase  in  other  morbid  signs 
(spread  of  sensory  and  of  visceral  affections)  will 
show  the  progress  of  the  ataxia  to  be  merely  one 
expression  of  a  general  advance  in  the  spinal  lesions 
and  will  serve  to  distinguish  it  from 

(b)  When  blindness   is   accompanied   by  mental 
deterioration.    Mott's  statement  that  fifty  per  cent 
of  early  optic  atrophies  develop  general  paralysis 
is  interesting  as  affording  a  possible  explanation  of 
cases  of  this  class. 


SYPHILITIC  CRANIAL  NERVES 


105 


Less  evident  but  no  less  certain  is  the  good  effect 
exerted  upon  pain  (Inglerans,  Dejerine)  and  deafness 
(Benenati)  by  the  improvement  in  the  mental  state  which 
follows  blindness. 

Diplopia  is  said  to  occur  in  about  forty  per  cent  of 
tabeticSo  With  the  exception  of  lightning  pains  it  is 


FIG.  43. — Paralysis  of  the  left  third  nerve.  The  tabetic  is  here  seen  trying  to 
look  to  the  right.  The  left  eye  rotated  outwards  but  the  right  remained 
immobile. 

often  the  earliest  symptom  which  tabetics  notice.  It  may 
last  only  a  few  seconds,  minutes,  hours,  or  days;  some- 
times even  weeks,  but  seldom  longer.  It  may  recur  un- 
expectedly. If  of  short  duration,  it  may  be  forgotten 
by  the  patient  unless  recalled  to, his  memory  by  ques- 
tioning. The  degree  of  disturbance  varies  from  blurring 
of  an  object  to  its  duplication.  Rarely  more  than  two 
images  are  seen. 

Sherrington  has  shown  that  the  visual  images  evoked 


106 


LOCOMOTOR  ATAXIA 


by  impulses  from  one  retina,  during  their  elaboration, 
remain  distinct  from  the  visual  images  which  are  evoked 
simultaneously  by  impulses  from  the  other  retina.  The 
resultant  of  the  images  from  the  one  retina  then  fuse 
with  that  from  the  other  to  produce  the  single  sensation 


FIG.  44. — Complete  paralysis  of  the  fourth  nerve  and  partial  paralysis  of  the 
third.  The  patient  could  not  move  her  eyes  upwards.  To  look  up  she 
tilted  back  her  head. 

of  binocular  vision.  When  the  binocular  mechanism 
contributes  two  resultants  not  such  as  we  normally  fuse, 
we  lose  binocular  vision;  two  distinct  sensations  arise, 
two  conscious  images  of  one  object. 

After  a  more  or  less  unsuccessful  attempt  to  fuse  the 
two  dissociated  images,  the  tabetic  ignores  the  false 
image;  suppresses  all  its  associations;  and,  at  the  cost 


of  the  binocular  quality,  recovers  his  visual  accuracy. 
Hence,  the  diplopia  is  transient. 

When  one  optic  nerve  is  partially  destroyed,  stimula- 
tion of  that  retina  may  result  in  few,  feeble  and  delayed 
impulses  passing  the  lesion.  These  impulses  evoke  vis- 
ual images  which  are  less  perfect  and  less  intense  than 
those  from  the  sound  eye.  Besides  thus  differing  in 
nature,  the  images  from  the  two  eyes  are  asynchronous ; 
hence  they  may  not  fuse.  When  the  site  stimulated  in 
one  retina  does  not  bear  the  usual  correspondence  to 
that  stimulated  in  the  other,  visual  images  which  are 
not  complementary  are  evoked  and  do  not  fuse.  Hence, 
diplopia  develops  when  the  accommodation  mechanism 
is  disturbed;  or  when,  owing  to  vestibular  lesions,  the 
coordination  of  the  eye  movements  fails;  or  when, 
through  implication  of  the  sensory  or  motor  innervation 
of  the  eye  muscles,  the  eye  movements  are  not  correlated. 
Examination  of  the  optic  nerve,  of  the  accommodation 
apparatus,  of  the  vestibular  nerve  and  of  the  eye  move- 
ments, will  disclose  the  underlying  factor  in  diplopia. 
The  diplopia  which  results  from  weakness  of  one  or  more 
of  the  external  muscles  of  the  eye,  consequent  upon 
syphilitic  lesions  in  the  nerve  supply,  is  accompanied 
by  abnormal  position  and  limitation  of  movement  of  the 
eye.  If  the  patient  comes  under  observation  while  suffer- 
ing from  diplopia,  the  candle  test  will  reveal  the  faulty 
muscle.  Usually,  however,  the  investigated  tabetic  has 
already  learnt  to  suppress  the  false  image.  Even  with 
evident  strabismus  there  may  be  no  diplopia.  Mirallie 
and  Desclaux  recommend  for  the  detection  of  the  sup- 
pressed image  the  use  of  a  conical  paper  tube,  25  cm. 
long,  4  cm.  in  diameter  at  the  base  and  1  cm.  in  diameter 
at  the  apex;  and  of  a  dark  colored  circular  patch,  3  cm. 


108 


in  diameter,  in  the  middle  of  a  large  white  card.  When 
the  card  is  5  or  6  meters  distant,  if  the  patient  who  has 
a  suppressed  image  places  the  base  of  the  cone  to  one 
eye  and  looks  at  the  dark  central  patch,  he  sees,  not  one, 


FIG.  45. — Complete  paralysis  of  the  right  sixth  nerve.  This  tabetic  is  trying 
to  look  to  the  right.  She  instinctively  turns  her  head  to  the  right,  her 
left  eye  rotates  imperfectly  to  the  right  (partial  left  third  palsy)  and  her 
right  eye,  instead  of  moving  outward,  remains  gazing  directly  forward. 

but  two,  patcheSo  The  amount  of  the  separation  of  the 
true  and  the  false  patches  and  their  relative  position  vary 
with  the  cause  of  the  diplopia. 

Instead  of  the  large  white  card,  I  used  a  white  screen 
in  which  concentric  circles  of  regularly  graded  diameter 
enclose  the  central  colored  patch,  and  radii  pass  from 
the  colored  patch  to  the  circumference  of  the  outermost 


SYPHILITIC  CRANIAL  NERVES 


109 


circle.     These  circles  and  radii  enable  the  position  of 
the  false  image  to  be  easily  denned. 

Of  twenty  tabetics,  without  refractory  errors  and  with- 
out conscious  diplopia,  seventeen  were  induced  by  this 


FIG,  46. — Complete  right  and  partial  left  ptosis  in  tabes. 

means  to  see  double ;  five  saw  double  when  the  tube  was 
placed  at  either  eye;  twelve  with  the  tube  at  one  eye, 
not  at  the  other;  nine  of  the  seventeen  gave  a  history 
of  diplopia,, 

The  internal  rectus  was  at  fault  eight  times;  the 
superior  oblique  thrice ;  the  external  rectus  twice ;  in  the 
remaining  four  I  could  not  with  certainty  determine  the 
erring  muscle. 


110  LOCOMOTOR  ATAXIA 

The  diplopia  tends  spontaneously  to  disappear.  So 
also  in  some  instances  does  the  strabismus.  Strabismus 
is,  as  are  all  other  motor  disabilities  of  tabes,  very 
amenable  to  psychotherapy.  Drooping  (ptosis)  and  re- 
traction of  the  eyelids  also  occur  in  tabes. 

Complete  lesions  of  the  fifth  nerve,  the  common 
sensory  nerve  of  the  face  and  of  the  buccal,  nasal,  ocular 
and,  in  part,  of  the  aural  mucous  membrane,  or  of  its 
sensory  roots,  are  rare.  So,  also,  are  lesions  of  the 
motor  root  which  supplies  the  muscles  of  mastication. 
But  partial  and  bilateral  sensory  disturbances  in  the  face 
are  more  common  than  is  generally  supposed.  There 
is  nothing  noteworthy  in  the  blunting  of  sensibility  de- 
tectable here  except  for  one  fact:  the  few  I  have 
examined  did  not  show  the  root  character  observable  in 
sensory  loss  in  other  regions. 

Absence  of  nausea  from  pharyrigeal  irritation,  absence 
of  pain  and  of  lid  closure  when  the  cornea  is  touched  are 
often  present  in  tabes.  The  sensory  paths  of  these  re- 
flexes are  not  yet  surely  identified. 

Rarely  facial  palsy  occurs.  It  may  appear  very  early 
in  tabes  and  is  usually  unilateral.  Fournier  mentions 
eight  cases  among  two  hundred  and  twenty-three  pre- 
ataxic  tabetics.  Unilateral  disturbances  of  muscles  which 
are  bilateral  and  which  habitually  function  together,  tend 
rapidly  and  spontaneously  to  disappear.  The  tabetic 
facial  palsy  is  characteristically  transient,  vanishing  in 
a  few  days  or  weeks.  Some  of  the  cases  described  are 
merely  results  of  banal  meningeal  inflammation.  The 
site  and  the  nature  of  the  condition  do  not  warrant 
fuller  discussion  here,  but  I  hope  later  to  publish  the 
data  I  have  collected  concerning  them. 

The  eighth  nerve  has  two  parts,  a  vestibular,  and  an 


SYPHILITIC  CRANIAL  NERVES  111 

auditory  or  cochlear.  Both  may  be  attacked  by  the 
spirochete.  The  source,  connections  and  functions  of 
the  vestibular  nerve  have  already  been  described  (pp. 
29  and  30).  Vestibular  lesions  are  more  frequent  than  au- 
ditory. They  may  occur  early  and  be  unilateral  or  bi- 
lateral. Lesions  of  the  vestibular  nerve  produce  loss  of 
muscular  tone  and  loss  of  the  sense  of  the  body's  posture. 
Hence  dizziness,  swaying,  diplopia,  nausea  and  other 
symptoms  arise.  Lesions  of  the  vestibular  nerve  are  de- 
tected by  three  tests:  a,  the  water  test;  b,  the  galvanic 
test ;  c,  the  rotatory  test. 

(a)  The  Water   Test:     The  head  is  maintained 
upright  and  the  ear  is  irrigated  for  twenty  seconds 
with  cool  or  warm  water. 

(b)  The  Galvanic  Test:     In  the  external  meatus 
or  on  the  tragus  of  the  ear  an  electrode  is  placed; 
the  other  electrode  may  be  applied  to  the  back  or  arm 
or  any  other  site  except  the  ear.    According  as  the 
anode  or  cathode  be  placed  to  the  ear,  the  result 
differs. 

(c)  The  Rotary  Test:     The  examined  person  is 
placed  in  a  revolving  chair  and  rotated  about  ten 
times  in  twenty  seconds. 

After  any  one  of  these  procedures  nystagmus  normally 
appears  and  persists  for  a  few  seconds.  From  the  pres- 
ence or  absence,  the  nature  and  the  direction  of  this  in- 
duced nystagmus  the  integrity  or  disturbance  of  the  ves- 
tibular function  is  determined.1 

Wittmaack  (1907)  induced  prolonged  auditory  fatigue 
in  groups  of  guinea  pigs.  Each  group  was  exposed  to 

'For  the  detailed  interpretation  of  the  varieties  of  induced  nys- 
tagmus in  vestibular  lesions  see  Barker's  "Monographic  Medicine,"  Vol. 
IV,  Appleton,  New  York. 


112  LOCOMOTOR  ATAXIA 

a  different  tone.  The  group  tone  was  sounded  in  the 
ear  of  the  guinea  pigs  frequently  and  periodically  for 
many  months.  The  guinea  pigs  were  then  killed,  and 
their  cochlear  membranes  and  nerves  were  examined 
histologically.  He  found  that  prolonged  overstimulation 
had  caused  the  cochlear  nerve  fibers  to  degenerate.  The 
bundle  which  degenerated  varied  with  the  tone ;  thus,  for 
a  tone  of  high  pitch,  a  certain  bundle  degenerated;  for 
a  tone  of  low  frequency,  another  bundle  degenerated. 
This  degeneration  began  in  the  sensory  membrane,  and 
spread  along  the  cochlear  nerve  toward  its  nucleus  in 
the  medulla. 

Habermann  examined,  by  histological  methods,  the 
sensory  membrane  and  cochlear  nerve  in  cases  of  defec- 
tive hearing  among  workers  in  noisy  trades.  He  was 
able  to  corroborate  Wittmaack's  results. 

Hence,  when  compound  aerial  waves  of  sound  are 
converted  into  nerve  impulses  at  the  cochlear  membrane, 
they  are  resolved  into  elemental  forms,  each  equivalent 
to  a  component  tone,  and  each  transmitted  along  a  sep- 
arate fiber  or  bundle  of  fibers  of  the  cochlear  nerve  to  the 
medulla.  Thence,  they  pass  to  the  cortex  to  excite,  in 
ordered  sequence,  images  of  tone. 

In  the  brain  the  elemental  tones  which  result  from  the 
disintegration  of  a  sound  at  the  cochlear  membrane,  are 
grouped  and  regrouped  until  the  final  synthesis  is  com- 
plete. Then  we  hear.  Only  a  musician  analyzes  what 
he  hears;  even  he  distinguishes  tones  seldom  and  con- 
sciously. Others  perceive  merely  the  end  result  of  a 
complex  mental  process. 

A  healthy  person  may  not  perceive  sound  waves  which 
impinge  upon  his  cochlear  membrane.  We  who  live  and 
think  in  noisy  cities  do  so  mainly  owing  to  this  power 


SYPHILITIC  CRANIAL  NERVES  113 

to  turn  a  deaf  ear.  We  experience  daily  in  ourselves, 
therefore,  a  deafness  due  to  distraction,  preoccupation, 
lack  of  attention. 

In  all  hearing  there  are,  thus,  two  factors,  a  psychic 
and  a  peripheral:  we  hear  among  the  sounds  wherein 
we  live  only  those  which  we  wish  to  hear,  only  those  to 
which  we  devote  attention. 

At  a  given  moment  we  may  not  hear,  owing  to  the 
competition  for  our  attention.  But  patients  who  have 
a  morbidly  restricted  power  of  attention  may  not  be  able 
to  hear  even  when  they  are  listening :  and  their  deafness 
is  remarkable  in  that  it  alters  with  the  amount  of  atten- 
tion available  at  the  moment  for  auditory  impressions. 
This  psychic  deafness  exists  normally  in  the  preoccupied 
and  in  the  old ;  and  pathologically  in  the  hysterical ;  and 
sometimes  in  the  tabetic. 

In  tabes,  one  or  both  auditory  nerves  may  be  impli- 
cated. The  sound  of  a  watch  ticking  may  be  heard  at  a 
greater  distance  from  one  ear  than  from  the  other:  it 
may  be  imperceptible  even  when  the  watch  is  in  contact 
with  the  ear.  The  vibration  of  a  tuning  fork  is  heard 
better  when  the  base  of  the  fork  is  in  contact  with  the 
mastoid  bone  than  when  the  vibrating  prongs  are  held 
near  the  ear;  bone  conduction  of  sound  is  better  than 
air  conduction :  therefore,  the  disturbance  of  hearing  is 
due  to  a  nerve  lesion.  When  the  tuning  fork  is  placed 
on  the  top  of  the  head  in  the  mesial  anteroposterior 
plane,  the  sound  is  heard  less  in  the  more  affected  ear. 
According  to  the  nature  of  the  fibers  destroyed,  percep- 
tion of  tuning  forks  of  various  pitch  is  lost.  With  de- 
struction of  certain  fibers,  tones  of  high  pitch  become 
inaudible;  with  destruction  of  others,  tones  of  low 


114  LOCOMOTOR  ATAXIA 

pitch  are  lost.  Together  with  this  loss,  subjective  noises 
may  occur. 

In  all  tabetic  lesions  of  the  auditory  nerve,  except  its 
extremely  rare  complete  destruction,  some  power  of 
hearing  must  persist ;  for  the  persistence  of  nerve  fibers 
means  persistence  of  the  ability  to  detect  the  tones  which 
these  fibers  subserve.  So  few  fibers  may  escape  that 
their  survival  is  undiscoverable  by  ordinary  routine 
methods  of  examination  and  can  be  detected  only  by  care- 
fully testing  the  apparently  deaf  tabetic's  hearing, 
throughout  the  range  of  the  auditory  scale  of  the  human 
ear,  by  means  of  the  Edelmann-Bezold  apparatus. 

In  the  auditory  nerve,  as  elsewhere,  the  tabetic  lesions 
cause  fewer,  feebler  and  imperfect  sensory  images.  Un- 
less he  particularly  focusses  his  attention,  the  afflicted 
tabetic  detects  only  a  sound  or  a  word  here  and  there. 
To  be  continually  on  guard,  to  strain  every  nerve  for 
chance  sounds  may  soon  prove  beyond  his  strength.  The 
occasional  meaningless  sounds  which  are  heard  are 
ignored,  for  it  is  speech,  not  isolated  words,  .which  com- 
mand attention.  Few  auditory  stimuli  are,  however, 
greater  to  a  person  than  the  sound  of  his  own  name,  or 
sounds  which  connote  things  intimately  related  to  his 
personality.  Hence  the  last  to  be  neglected  are,  as  a 
rule,  the  personal  sounds:  they  can  be  lightly  heard  by 
the  tabetic  even  when  impersonal  topics  must  be  com- 
municated by  shouting. 

Sound  must  be  endowed  with  this  inherent  interest 
or  with  a  considerable  degree  of  loudness,  or  with  a 
certain  imperative  quality,  before  the  tabetic  may  become 
conscious  of  it.  Below  this  threshold  he  is  deaf.  If 
the  hearing  retained  be  not  wholly  inadequate  for  the 
rougher  needs  of  life,  the  tabetic  may  become  more  or 


SYPHILITIC  CRANIAL  NERVES  115 

less  resigned  to  his  deafness.  If  hearing  be  too  impaired 
to  permit  a  satisfying  amount  of  communication  with  the 
world  of  sounds,  and  especially  if  subjective  sounds 
occur,  the  consequences  vary  according  to  the  mental 
state  of  the  tabetic.  The  uncertainty  and  effort  which 
accompany  his  striving  to  hear  fatigue  and  depress 
him;  and  hearing  shares  in  the  depreciation  which  all 
cerebral  functions  suffer  in  such  unfavorable  mental 
states.  Even  if  the  lesion  be  stationary  the  deafness 
tends  to  increase. 

t)eafness  is  less  in  interest  than  in  apathy  and  in 
favorable  than  in  unfavorable  mental  states.  Psycho- 
therapy can  often  procure  considerable  improvement  in 
hearing.  Deafness  depends  not  only  on  the  tabetic  le- 
sions in  the  auditory  nerve,  but  also  upon  the  mental 
state.  The  amount  of  deafness  is  an  inaccurate  guide 
to  the  extent  of  the  destruction  of  the  auditory  nerve,  a 
misleading  index  to  the  actual  capacity  to  hear. 

The  ninth  or  glossopharyngeal  nerve  is  occasionally 
implicated  for  loss  of  taste  may  occur. 

There  is  nothing  to  distinguish  syphilitic  lesions  of 
the  eleventh  or  spinal  accessory  nerve,  the  nerve  of 
supply  of  the  trapezius;  or  lesions  of  the  twelfth,  the 
hypoglossal  nerve,  the  nerve  of  supply  of  the  tongue, 
from  analogous  lesions  of  motor  nerves  elsewhere. 

Invasion  of  the  vagus  is  very  frequent.  With  the  sym- 
pathetic the  vagus  constitutes  the  vegetative  nervous 
system.  Its  implication  in  tabes  will  be  considered  in 
the  next  two  chapters. 


CHAPTER  VI 

RESULTS  OF  THE  SYPHILITIC  LESIONS  OF  THE  VEGETA- 
TIVE   NERVOUS    SYSTEM 

a.  SENSORY  AND  MOTOR  DISTURBANCES 

The  correlation  of  cells.  Development  of  the  primitive  vegetative 
nervous  system.  The  vegetative  nervous  system  in  man  composed 
of  two  antagonistic  components,  the  vagal  and  the  sympathetic. 
Action  of  these  components  illustrated  by  the  pupil.  The  pupil 
in  tabes.  Vegetative  reflex  arcs  and  plexuses.  The  afferent  and 
efferent  fibers  linking  these  arcs  with  so-called  "centers"  in  the 
central  nervous  system.  Tracing  of  the  sensory  fiber.  Proof  that 
pain  from  pressure  on  the  face  passes  not  by  the  fifth  but  by  the 
sympathetic.  Pressure  pain  loss  in  tabes  on  limbs,  eyes,  testicles 
and  other  viscera.  Loss  of  visceral  reflexes.  Lightning  pains, 
character  and  frequency.  Their  source  in  irritation  of  the  vege- 
tative nervous  system.  Lightning  pains  and  crises  allied  phenom- 
ena. Gastric,  rectal,  bladder  and  genital  crises.  Pains  and 
crises  reciprocally  related  to  the  mental  state.  The  physiology  of 
micturition.  Micturition  in  tabes. 

THE  activity  of  the  individual  cell  is  governed  by  its 
nucleus.  In  aggregations,  the  cells  specialize ;  some  pro- 
cure, others  digest,  others  convey  food  necessary  to  the 
existence  of  the  colony.  The  more  highly  differentiated 
the  cells  are,  the  less  do  they  depend  for  their  needs 
upon  their  individual  efforts,  the  more  is  the  activity  of 
the  various  cells  correlated  to  the  needs  of  the  whole 
colony. 

This  correlation  is  earliest  attained  by  chemical  and 
mechanical  action.  Nutritive  fluids  are  circulated 
through  the  colony  by  cilia  and  by  contractile  tubes ;  the 
various  cells  withdraw  what  they  need,  and  excrete  into 
the  circulating  fluid  substances  which  stimulate  the  activ- 

116 


ity  of  their  fellows.  Then  nerve  cells  are  differentiated 
to  preside  over  these  vital  activities.  They  send  fibers 
among  the  other  cells.  At  the  ends  of  these  nerve  fibers, 
chemical  and  mechanical  action  is  converted  into  nerve 
energy  which  passes  along  fibers  to  the  body  of  the 
nerve  cell.  From  this  presiding  nerve  cell,  impulses  pass 
by  other  fibers  to  be  distributed  throughout  the  organism 


v=s 


FIG.  47. — Diagrams  to  show  the  effect  on  the  pupil:  1,  of  stimulation  of  the 
sympathetic  (S  + )  or  paralysis  of  the  vagal  (V  — )  fibers;  2,  of  the  balanced 
(V  =  S)  action  of  sympathetic  and  of  vagal  stimulation;  and  3,  of  paralysis 
of  the  sympathetic  (S  — )  or  of  stimulation  of  the  vagal  (V  + )  fibers. 

to  provoke  chemical  and  mechanical  changes.  These 
presiding  or  ganglion  cells  and  their  fibers  constitute  the 
primitive  vegetative  nervous  system  through  which  the 
breaking  down  or  building  up  of  the  protoplasm  in  the 
multicellular  organism  is  correlated  more  speedily,  more 
powerfully,  and  more  accurately  than  by  direct  mechani- 
cal or  chemical  action. 

In  man,  the  vegetative  system  is  composed  of  cells 
which  during  embryonic  life  wander  from  the  ventral 
part  of  the  neural  canal  towards  the  periphery. 

Among  the  vegetative  fibers,  two  antagonistic  groups 
are  said  to  be  distinguishable  in  practically  every  organ ; 
one,  a  stimulating  or  accelerator  group,  the  autonomic 
or  vagal  group ;  the  other,  an  inhibitory,  the  sympathetic 
group.  Thus,  in  the  pupil,  stimulation  of  the  vagal 


118 


LOCOMOTOR  ATAXIA 


fibers  causes  contraction  of  the  sphincter  of  the  iris  and 
produces  a  small  pupil  (Fig.  47).  Stimulation  of  the 
sympathetic  fibers  causes  contraction  of  the  dilatator  of 
the  iris  and  produces  enlargement  of  the  pupil  (Fig.  47). 

A  small  pupil  may  result 
either  from  stimulation  of 
the  vagal  fibers  or  from 
paralysis  of  the  dilating 

FiG.48.-Retractionofthelids,eccen-     fibers  of  the  sympathetic; 
trie  pupils.    (Montefiore  Hospital    a  large  pupil,  from  paral- 

case.)  •         •    .1  i     .CT. 

ysis    of   the   vagal   fibers 

(for  example  by  atropin  or  belladonna)  or  by  stimula- 
tion of  the  sympathetic.  Usually  these  antagonistic  ten- 
dencies more  or  less  balance  one  another  (Fig.  47). 
Variations  in  the  size  of  the  pupil  express  the  oscillations 
in  this  balance. 

The  pupil  changes  which  occur  in  tabes  are  of  three 
kinds:  changes  in  shape,  in  size,  and  in  reflex  activity. 
The  normally  circular  pupil  may  become  irregular, 
usually  first  during  ac- 


.    49.-Tabetic    with    left    pupQ 
widely,  right  moderately  dilated. 


tion,  later  when  at  rest 
also.  The  irregular  pupil 
from  vagal  irritation  be- 
comes usually  smaller  (3, 

Fig.     47),     occasionally 

from  sympathetic  irrita- 
tion, larger  (1,  Fig.  47),  than  its  fellow.  This  irregular 
pupil  of  altered  size  more  and  more  slowly  and  feebly 
contracts  when  illumination  increases,  or  dilates  when 
darkness  occurs.  The  pupil  ultimately  becomes  fixed, 
immobile,  during  changes  in  light,  but  it  still  narrows 
during  near,  and  dilates  during  far,  seeing.  Such  a  pupil, 
inactive  to  light,  responsive  to  accommodation  was  first 


RESULTS  OF  SYPHILITIC  LESIONS        119 

described  by  Argyll-Robertson  of  Edinburgh,  and  is 
after  him  named  the  Argyll-Robertson  pupil.  It  is  prac- 
tically pathognomonic  of  syphilis  of  the  nervous  system, 
of  which  it  usually  is  the  first  sign.  The  course  of  this 
light  reflex  is  still  in  doubt. 

The  typical  tabetic  pupil  is  a  pin-point  pupil,  the  result 
of  unbalanced  action  of  the  vagal  fibers.  When  these 
vagal  fibers  are  destroyed  the  pupil  may  dilate,  owing  to 
the  unopposed  action  of  the  sympathetic. 

The  cells  of  the  vegetative  nervous  system  are  linked 
by  their  processes  to  form  reflex  arcs.  These  vegetative 
reflex  arcs  are  linked  in  plexuses  which  are  associated 
with  a  view  to  their  collaboration  in  functions  common 
to  them.  Thus  in  the  intestinal  wall  are  the  associated 
plexuses  of  Meissner  and  of  Auerbach.  Through  their 
correlated  activity,  while  one  portion  of  the  muscular 
tube  of  the  intestine  contracts,  the  succeeding  portion  is 
caused  to  dilate ;  so  the  passage  onwards  of  the  intestinal 
contents  is  facilitated.  As  the  threshold  of  each  reflex 
arc  which  forms  a  link  in  this  plexus  chain  is  lowered  in 
sequence,  the  waves  of  contraction  pass  along  the  muscu- 
lar tube  of  the  intestine  in  the  same  direction,  in  regular 
order,  and  at  an  uniform  rate.  This  reflex  correlation  is 
wiiolly  peripheral:  it  persists  after  all  connection  with 
the  central  nervous  system  has  been  severed. 

From  the  plexuses,  fibers  conveying  afferent  impulses 
to  the  central  nervous  system  pass  along  posterior  nerve 
roots  and  homologous  paths,  to  where  in  the  central  nerv- 
ous system  cell  groups  occur,  sometimes  called  centers, 
from  which  small  white  medullated  fibers  arise.  These 
small  wThite  fibers  leave  the  pons,  medulla  and  spinal  cord 
by  the  anterior  nerve  roots,  or  by  their  cranial  represen- 
tatives, to  proceed  to  the  periphery,  along  blood  vessels 


120 


LOCOMOTOR  ATAXIA 


or  nerves,  till  they  form  a  synapse  with  cells  in  a  near 
or  remote  ganglion  of  the  vegetative  nervous  system. 
From  such  a  synaptic  cell  a  non-medullated  or  gray  fiber 
conveys  the  spinal  impulses  to  their  destination  in  liver 

or  other  gland,  in 
intestine  or  other 
involuntary  muscle. 
Chemical  and  me- 
chanical stimuli,  af- 
fecting the  termina- 
tions of  the  vegeta- 
tive fibers  in  the 
viscera,  are  convert- 
ed into  nerve  im- 
pulses which  may, 
in  part,  pass  back  to 
the  central  nervous 
system;  and  in  cells 
there  evoke  im- 
pulses which,  re- 
turning to  the  stim- 
ulated site  or  to  al- 
lied sites,  accelerate 
or  inhibit  the  activ- 
ity of  the  peripheral 
reflex  arcs  of  the 
vegetative  nervous 
system.  Thus  may 

be  correlated  the  vegetative  activities  of  the  several  seg- 
ments of  the  body. 

But  these  usually  unperceived  impulses  which  arise 
from  visceral  stimulation,  when  they  are  of  extraordi- 
nary intensity,  may  reach  consciousness.  We  feel  tumul- 


FIG.  50. — Extirpation  of  Gasserian  ganglion. 
The  resulting  area  of  anesthesia  to  light 
touch  is  shown  by  the  continuous  line  and 
to  65  gm./dm.2  pressure,  by  the  dotted  line. 
Note,  that  although  there  is  complete  loss 
of  common  sensibility  within  the  area  of 
the  distribution  of  the  fifth  nerve,  sensi- 
bility to  moderate  pressure  touch  is  lost  only 
on  the  forehead  and  around  the  eye. 
(Maloney  and  Kennedy.) 


KESULTS  OF  SYPHILITIC  LESIONS        121 


tuous  heart  action,  abnormal  peristalsis  in  the  intestines, 
and  other  visceral  changes,  as  discomfort  or  even  pain. 

Some  state  that  the  fiber  which  conveys  discomfort  or 
pain  from  a  viscus  originates  in  the  bipolar  cell  of  a 
spinal  ganglion.  The  truth  or  falseness  of  this  is  difficult 
to  establish.  The 
Gasserian  ganglion 
of  the  fifth  cranial 
nerve  is  the  homo- 
logue  of  the  pos- 
terior root  gan- 
glion. In  extirpa- 
tion of  the  Gasser- 
ian ganglion  loss 
of  touch,  of  pin- 
prick pain  and  of 
sensitivity  to  light 
pressures  occurs 
on  the  forehead, 
cheek,  lips,  nasal, 
buccal  and  lingual 
mucous  membranes 
supplied  by  the 
£fth,  but  either  no 
or  only  partial  loss 
of  pressure  pain. 

Pain  can  always 
be  still  elicited  by 
pressure,  but  the  loss  on  the  cheek  is  constantly  less  than 
that  on  the  forehead,  on  the  lips  than  on  the  cheek,  and 
the  tongue  enjoys  greater  immunity  than  all  of  these 
sites.  Sometimes  the  forehead  alone  shows  loss:  the 
cheek  is  never  affected  unless  the  forehead  also  is;  nor 


FIG.  51. — Extirpation  of  the  Gasserian  ganglion, 
to  show  distribution  of  loss  of  pain  on  pres- 
sure. Outside  the  affected  area  pain  was 
felt  when  a  pressure  of  1  ^  kilos  per  unit  area 
was  applied;  inside,  pressures  varying  from 
3  to  8  kilos  were  needed  to  evoke  pain.  The 
pressure  analgesia  is  greatest  on  the  fore- 
head and  less  on  the  chin  than  on  the  cheek. 
(Maloney  and  Kennedy.) 


122  LOCOMOTOB  ATAXIA 

the  tongue,  if  the  cheek  escapes.  Immediately  after 
operation,  the  pressure  pain  loss  is  greatest  but  recovery 
is  rapid  and  often  perfect. 

As  complete  extirpation  of  the  ganglion  may  leave  the 
pressure  pain  sense  normal,  the  fibers  which  conduct 
that  sense  do  not  have  their  origin  in  the  ganglion.  Any 
loss  of  pressure  pain  produced  by  removal  of  the  Gas- 
serian  ganglion  must,  therefore,  be  due  to  accidental 
injury  of  some  nerve  mechanism  whose  fibers  in  varying 
number  enter  the  field  of  operation. 

Injuries  of  the  seventh  nerve,  peripheral  to  the  Fallo- 
pian canal,  produce  atrophy  of  the  facial  muscles  but  no 
loss  of  common  sensibility ;  whereas  injury  to  the  seventh 
in  the  Fallopian  canal  may  be  associated  in  the  skin, 
muscles  and  bones  of  the  facial  muscular  apparatus  with 
loss  of  pain  produced  by  pressures  up  to  four  kilos  per 
unit  area.  In  the  area  of  this  loss  of  pressure  pain,  the 
sensibility  to  touch,  pin-prick  and  light  pressure  is  per- 
fect; the  sensibility  of  the  fifth  nerve  and  its  branches 
is  unimpaired. 

Section  of  the  hypoglossal  in  the  neck  produces  atro- 
phy, but  no  loss  of  pressure  pain  in  the  tongue. 

Fibers  which  do  not  belong  to  the  fifth  nerve;  which 
are  common  to  the  forehead,  cheek,  lips  and  tongue; 
which  invariably  occur  in  the  region  of  the  fifth  nerve 
roots  and  of  the  Gasserian  ganglion;  which  are  there  in 
greater  proportion  from  the  forehead  than  from  the 
tongue;  and  which  anastomose  so  perfectly  that  the 
isolated  total  destruction  of  the  fibers  from  one  site  is 
practically  impossible — such  fibers  can  belong  only  to 
the  vegetative  nervous  system.  The  vegetative  nervous 
system  must  conduct  the  pressure  impulses  which  evoke 


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124 


LOCOMOTOR  ATAXIA 


in  consciousness  the  sensation  of  pain  from  pressure  on 
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As  the  Gasserian  ganglion  neither  gives  origin  to 
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perhaps  the  spinal  root  ganglion  is  equally  unrelated  to 
the  corresponding  vegetative  fibers  from  the  trunk,  limbs 
and  viscera. 

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FIG.  55. — This  diagram  represents  the  relations  of  the  spinal  sympathetic 
fibers  as  analogous  to  those  of  the  sympathetic  fibers  of  the  head.  Thus, 
the  sympathetic  fiber  conveying  non-sentient  and  sentient  sensory  im- 
pulses from  vessels,  glands  and  non-striped  muscle,  to  the  spinal  cord,  is 
depicted  as  originating  apart  from  the  posterior  root  ganglion. 

pain  of  claudication  can  be  abolished  by  dissecting  the 
sympathetic  from  the  thickened  walls  of  the  blood  vessels 
of  the  limbs. 

In  tabes,  the  vegetative  fibers  conducting  pressure 
pain  either  because  of  lesions  in  their  peripheral  course 
or  through  implication  in  the  posterior  root  lesion,  may 
be  .partially  or  completely  destroyed. 

In  the  face,  the  normal  pressure,  per  unit  area,  which 
elicits  pain  is  1^  to  1  kilo.  In  tabes,  loss  of  pressure 
pain  is  occasionally  met  greater  than  that  which  occurs 


RESULTS  OF  SYPHILITIC  LESIONS        125 

in  section  of  the  fifth  nerve  or  roots,  after  extirpation 
of  the  ganglion,  and  in  nuclear  lesions ;  and  greater  than 
that  seen  in  any  seventh  nerve  or  nuclear  lesion.  I  have 
examined  not  a  few  tabetics  in  whom  pressures  as 
high  as  15  kilos  per  unit  area,  pressures  at  which  one 
desists  lest  the  tissues  be  injured,  could  be  applied  to 
the  forehead,  zygoma  and  cheeks  without  eliciting  pain. 
This  loss  of  pain  on  pressure  in  the  face  occurs  without, 
or  with,  disturbance  of  common  sensibility. 

As  a  rule,  loss  of  pressure  pain  appears  first  in  the 
peroneal  region  of  the  lower  limbs.  It  is  there  one  of 
the  early  sign's  of  tabes.  This  loss  may  at  first  be  evident 
in  a  unilateral  raising  of  the  pressure  pain  threshold; 
on  the  sound  limb,  over  the  Achilles  tendon,  alongside 
the  feeling  of  pressure,  pain  may  develop  when  a  pres- 
sure of  about  3  kilos  per  unit  area  is  applied,  whereas  on 
the  affected  limb  the  threshold  may  be  5,  6,  or  more 
kilos.  Soon  the  loss  may  become  bilateral,  then  equal; 
and  often  no  degree  of  pressure  will  elicit  pain.  Indeed, 
ulcers  over  points  subject  to  pressure  may  develop  pain- 
lessly :  and  fractures  of  the  bones  may  occur  without  even 
discomfort.  In  the  arms  the  loss  usually  first  appears 
on  the  ulnar  side  of  the  forearm,  in  the  area  where  reflex 
pain  of  cardiac  origin  occurs,  in  the  area  closely  asso* 
ciated  with  the  region  of  the  spinal  cord  from  which 
the  ciliospinal  fibers  arise. 

The  loss  of  pressure  pain  is  not  confined  to  the  face, 
limbs  or  trunk.  The  commonest,  and  often  the  only, 
sign  of  sensory  disturbance  in  the  head  is  loss  of  pain 
on  pressure  of  the  eyeballs.  On  compressing  the  eye, 
besides  absence  of  pain,  there  is  also  absence  of  the 
normal  slowing  of  the  hearf's  rate.  The  testicle  may  be 
compressed  as  much  as  due  regard  for  its  integrity 


126  LOCOMOTOR  ATAXIA 

permits,  without  inducing  pain.  Pressure  in  the  epigas- 
trium may  elicit  no  sensation.  Parturition  may  be  pain- 
less. 

Preceding  the  loss  of  pain  on  pressure,  later  accom- 
panying it,  and  still  later  disappearing,  is  the  most 
constant  and  usually  the  earliest  sign  of  tabes,  sponta- 
neous pain. 

This  pain  may  sometimes  have  a  root  distribution. 
Usually  the  patient  when  asked  to  show  where  his  pain 
lies  moves  his  indicating  hand  vaguely  up  and  down  his 
leg.  Pain  may  appear  suddenly  and,  after  a  time,  either 
as  suddenly  vanish  or  gradually  cease.  Or  it  may  be 
more  or  less  continuously  present  and  subject  to  un- 
expected exacerbation.  It  may  occur  at  all  times  of  the 
day:  it  may  awake  the  sleeping  tabetic.  It  may  be  a 
mild  neuralgic  pain  which  is  mistaken  for  rheumatism, 
or  a  pain  of  insupportable  severity. 

Usually  it  first  appears  in  one  leg,  maybe  in  both,  less 
often  in  the  back,  arms,  or  face.  As  a  rule,  the  pain 
shoots  down  the  back  of  the  thigh  to  the  calf,  terminating 
sometimes  there,  sometimes  in  the  heel,  sometimes  in 
a  toe.  It  may  be  localized  to  isolated  areas  of  muscle 
as  if  fragments  were  being  cut  out  or  torn  out.  Some- 
times the  pain  is  like  that  from  a  stab  or  a  twisting  in 
the  flesh  of  a  sharp  instrument ;  sometimes  it  is  described 
as  tearing  or  rending. 

The  sudden,  excessive,  diffuse  and  persistent  nature 
of  the  pain  is  reminiscent  of  the  so-called  thalamic,  or  of 
the  protopathetic,  response  to  peripheral  painful  stimuli. 
It  is  doubtless  due  to  an  irritation  of  the  central  end  of 
diseased  fibers,  as  it  can  be  associated  with  loss  of  sen- 
sibility to  painful  stimuli.  Its  localization  may,  there- 
fore, be  hallucinatory,  like  the  pain  felt  in  amputated 


RESULTS  OF  SYPHILITIC  LESIONS        127 

toes;  but  sometimes  the  painful  area  is  hypersensitive 
even  to  the  slightest  pressure.  The  fibers  which  conduct 
this  pain,  in  part,  may  belong  to  the  common  sensory 
system,  but  in  part  also,  if  not  mainly,  belong  to  the 
vegetative  system;  they  are  probably  sympathetic  in 
origin.  Sweating,  pallor,  or  blushing,  and  edema  of  the 
painful  area  may  accompany  the  attack,  and  afford  fur- 
ther proof  that  the  vegetative  nervous  system  is  irri- 
tated. 

When  bouts  of  pain  occur  not  in  limbs  but  in  viscera, 
they  are  called  tabetic  crises.  Their  nature  is  every- 
where the  same;  a  sudden  pain,  diffuse  or  radiating  in 
character,  which  attains,  almost  immediately,  its  maximal 
intensity,  which  is  accompanied  by  vascular,  secretory 
and  motor  phenomena  and  which  suddenly,  sometimes 
gradually,  ceases  and  recurs. 

Attacks  of  pain  associated  with  vascular  and  secretory 
changes  occurring  in  the  eye  region  have  been  de- 
scribed by  Knauer,  Spiller  and  others.  Of  the  similar 
attacks  occurring  at  other  sites,  the  best  known  is  the 
gastric  crisis.  The  gastric  crisis  consists  of  nausea  and 
vomiting,  preceded  by  stabbing  pains  radiating  forward 
from  the  middle  of  the  back,  or  by  cramping  pains  espe- 
cially in  the  right  hypochondrium,  or  by  discomfort  or 
burning  pain  in  the  epigastrium,  or  by  eructations.  The 
pain  may  closely  simulate  that  seen  in  gastric  ulcer  or  in 
gall  stone  or  in  appendicitis,  and  may  lead  to  the  harm- 
ful employment  of  futile  surgical  measures.  The  vomit- 
ing may  or  may  not  relieve  the  pain  or  discomfort;  it 
may  start  unheralded  and  may  be  almost  free  from 
nausea.  X-ray  photographs  of  the  phenomenon  show  a 
diminution  of  the  stomach  shadow  and  antiperistaltic 
movements  just  as  in  vomiting  from  other  causes.  The 


128  LOCOMOTOR  ATAXIA 

stomach  contents  are  rejected  sometimes  with  great 
violence :  then  the  vomit  may  be  mucoid  or  frothy.  In 
severe  attacks  the  vomit  is  colored  yellow  or  green  by 
bile;  and  sometimes  it  is  coffee  colored  by  blood. 

The  vomiting  usually  lasts  a  few  minutes ;  recurs  after 
an  hour  or  more ;  and  may  be  repeated  five  or  six  times 
for  a  day,  sometimes  for  two  days.  Then  a  quiescent 
period  of  months  or  longer  may  ensue. 

The  crisis  may  be  precipitated  by  a  drug  such  as 
pilocarpin,  which  stimulates  the  vagus.  During  the  gas- 
tric crisis  symptoms  of  vagal  irritation  are  evident: 
the  pupils  become  pinpoint;  a  characteristic  laryngeal 
stridor  is  often  heard  which  enables  the  vomiting  of 
gastric  crises  to  be  distinguished  audibly  from  other 
forms;  and  intestinal  colic  and  diarrhea  may  occur. 
The  crisis  is,  therefore,  due  to  a  diffuse  vagal  irritation 
with  its  storm  center  in  the  vagal  fibers  which  supply  the 
stomach. 

In  cases,  fortunately  not  common,  no  provocation  of 
the  crisis  can  be  traced.  Concomitant  increase  of  the 
signs  of  vestibular  or  of  vagal  lesions  may  occasionally 
show  the  crisis  to  be  a  manifestation  of  an  active  exten- 
sion of  the  syphilitic  invasion.  The  process  of  extension 
soon  ends.  Degeneration  succeeds  irritation,  and  the 
crisis  stops.  In  other  cases,  dietetic  errors,  or  mental 
stress,  aggravate  a  chronic  irritability  of  the  vagus 
which  is  evident  in  hyperacidity,  eructations,  nausea,  and 
intestinal  phenomena.  In  other  cases  again  psycho- 
analysis reveals  a  mental  incentive  to  nausea,  which  pre- 
cipitates the  attack.  The  tracing  of  the  immediate  cause 
of  the  crisis  is  seldom  difficult. 

The  amount,  nature,  and  frequency  of  the  vomiting, 
and  the  patient's  weight  are  the  guide  to  the  severity 


RESULTS  OF  SYPHILITIC  LESIONS        129 

of  the  crises.  The  crises  are  self-limiting  and  tend 
spontaneously  to  disappear.  In  some  tabetics  crises  are 
frequent,  in  others  rare,  in  others,  again,  unknown. 

Gastric  crises,  just  as  pain  crises,  have  a  large  mental 
element  in  their  production. 

With  gastric  crises  urgency  of  defecation  and  tenesmus 
may  occur.  Sometimes  these  rectal  crises  appear  alone ; 
the  tenesmus  is  most  distressing,  and  bloody  stools  occur. 
The  commonest  type  of  intestinal  disturbance  is  spastic 
constipation  periodically  alternating  with  diarrhea,  a 
disturbance  often  seen  also  in  non-tabetics  suffering  from 
vagal  irritability.  During  the  diarrheal  attacks,  or  dur- 
ing diarrhea  produced  by  the  use  of  drugs,  leakage  of 
the  intestinal  contents  may  occur,  often  so  slight  that 
the  tabetic  attributes  it  to  his  carelessness  and  does 
not  consider  it  worthy  of  mention. 

In  early  tabes,  irritation  of  the  sensory  nerves  of  the 
bladder  may  cause  an  imperious  demand  for  immediate 
evacuation  of  urine,  accompanied  sometimes  by  a  spas- 
modic retention  of  urine :  the  urgent  desire  to  micturate 
sometimes  cannot  be  satisfied,  and  when,  by  straining 
and  by  attitudinizing,  urination  is.  induced,  exaggerated 
general  shivering  or  pain  may  occur  during  the  enforced 
act.  Preceding  and  accompanying  urgency  of  micturi- 
tion is  often  a  sudden,  intense  and  shooting  pain  which 
radiates  along  the  penis  and  into  the  testicle,  sometimes 
into  the  perineum.  While  the  pain  lasts  the  difficulty  of 
micturition  may  be  tremendous.  An  agonizing  effort 
may  result  only  in  a  few  drops  of  blood-stained  urine. 
During  such  an  attack  I  found  that  the  temperature  of 
the  urine  as  it  issued  from  the  meatus  was  1.2°  F.  higher 
than  the  mouth  temperature.  After  this  attack  the  tern- 


130  LOCOMOTOR  ATAXIA 

perature  of  the  urine  was  0.4°  F.  higher  than  that  of 
the  mouth. 

The  asocial  influence  of  these  excretory  disturbances 
is  obvious;  their  effect  upon  the  mental  state  of  the 
patient  is  sometimes  profound.  A  tabetic  who  was  under 
my  care  in  the  Post-Graduate  Hospital  had  urgency  of 
urination  and  defecation,  loss  of  one  Achilles  jerk?  pin- 
point pupils,  and  some  hypalgesia  in  the  legs.  He 
walked  miles  out  of  his  way,  to  and  from  his  work,  that 
he  might  pass  many  places  where  he  could  seek  imme- 
diate relief  when  the  desire  to  evacuate  assailed  him. 
He  became  so  emaciated  and  exhausted  from  anxiety  and 
from  the  exertion  of  walking,  that  he  could  hardly  stand. 
A  fortnight  of  rest  and  of  evacuating  at  frequent  regular 
intervals  restored  him. 

Occasionally  genital  crises  also  arise.  Slight  periph- 
eral irritation  produces  persistent  and  painful  erections. 
The  frequency  with  which  sexual  excess  is  blamed  for 
the  onset  of  tabes  suggests  that  an  irritative  condition 
of  the  pudic  nerve  may  often  be  an  early  state  of  tabes. 
With  the  development  of  anesthesia,  loss  of  satisfaction 
may  occur.  Lack  of  sexual  power  develops,  partly  due 
to  interruption  of  the  reflex  arcs;  mainly,  however,  not 
to  physical  but  to  psychic  causes.  The  blind  tabetic 
usually  remains  potent.  Ataxies,  while  being  success- 
fully trained  to  walk,  frequently  volunteer  that  they  are 
recovering  virility.  One  of  my  ataxic  patents,  H.,  for 
eight  years  a  tabetic,  for  three  impotent,  with  urinary 
incontinence,  on  his  recovery  from  ataxia,  in  spite  of 
my  protests,  married. 

Pains  and  crises  are  worse  in  fatigue,  depression  and 
fear;  in  the  seeing  than  in  the  blind  (Inglerans,  Dejer- 


KESULTS  OF  SYPHILITIC  LESIONS        131 

ine  and  others) ;  in  ataxies  untrained  to  coordinate 
movement  than  in  those  trained. 

The  pains  or  crises  may  last  for  years  before  any 
other  symptoms  are  detectable.  Indeed,  some  clinicians 
distinguish  types  of  tabes  in  which  pains  and  gastric 
crises  predominate.  If  the  disease  advances,  the  irrita- 
tion may  be  followed  by  destruction;  pains  and  crises 
then  dimmish  and  may  be  succeeded  by  paralytic  phe- 
nomena. 

Normally  the  muscular  wall  of  the  bladder  contracts 
reflexly  upon  its  contents  at  regularly  recurring  inter- 
vals. As  the  bulk  of  the  contents  increases  the  more 
powerful  and  more  frequent  these  reflex  contractions 
become,  until  they  reach  an  intensity  at  which  the  con- 
traction of  the  sphincter  closing  the  bladder  is  inhibited ; 
the  urine  is  then  propelled  along  the  urethra  to  the 
exterior  by  a  tonic  contraction  of  the  bladder  wall.  In 
the  act  of  expelling  urine  from  the  bladder,  the  dia- 
phragm is  fixed,  and  the  abdominal  wall  contracts,  so 
that  the  general  intra-abdominal  pressure  is  increased  to 
reinforce  the  expulsive  power  of  the  contracting  bladder 
wall. 

During  infancy  the  bladder  fills  and  empties  reflexly. 
We  are  trained  to  consciousness  of  the  act  of  micturition 
and  taught  to  inhibit  the  act  in  conformity  with  social 
usage.  The  inhibition  of  the  bladder  reflexes  produces 
discomfort.  This  discomfort  must  arise  periodically 
when  the  bladder  wall  contracts  on  its  contents,  yet  we 
are  not  normally  subject  to  sudden  and  regularly  re- 
curring demands  to  micturate.  The  intermittent  sen- 
sory stimuli  from  the  contracting  distended  bladder,  in 
their  passage  to  consciousness,  are  mitigated  and  made 
continuous;  and  they  gradually  increase  in  their  power 


132  LOCOMOTOR  ATAXIA 

to  command  attention  as  the  bladder  fills  till  the  sensa- 
tion they  evoke  prevails  over  other  interests. 

The  call  to  urinate  prevails  at  a  moment  which  depends 
not  only  upon  the  bulk  of  the  bladder  contents  but  upon 
environmental  conditions.  Where,  as  in  war,  the  satis- 
fying of  natural  impulses  is  dangerous,  the  bladder  will 
tolerate  for  hours  urine  in  quantities  which  under  safer 
circumstances  would  demand  immediate  evacuation. 

Once  urination  has  begun,  it  tends  reflexly  to  continue 
till  the  bladder  is  empty.  Only  the  adult  can  interrupt 
the  act  and  he,  it  may  be,  not  successfully. 

As  the  bladder  develops  from  both  allantois  and  cloaca, 
its  sensory  nerves  pass  through  both  lumbar  and  sacral 
posterior  nerve  roots.  If  these  roots  are  affected  by  a 
tabetic  lesion,  the  sensory  impulses  become  fewer,  feebler; 
and  delayed.  As  the  sensory  loss  increases,  the  bladder 
must  contain  a  greater  and  greater  quantity  of  urine 
before  the  need  for  evacuation  becomes  perceptible; 
while  the  urine  flows,  the  tabetic  may  experience  no 
sensation  of  its  passage,  and  during  evacuation  the 
desire  to  micturate  may  be  satisfied  before  the  bladder 
is  emptied. 

Loss  of  sensibility  similar  to  that  present  in  the  blad- 
der and  the  urethra  may,  though  usually  later,  be  found 
also  on  the  perineum  and  in  the  vagina  and  rectum. 

The  anesthesia  of  the  urinary  tract  removes  the  only 
incentive  to  urination  that  the  adult  acknowledges;  it 
abolishes  also  the  demand  for  complete  emptying.  The 
tabetic,  therefore,  urinates  more  and  more  seldom;  and 
he  less  and  less  completely  empties  his  bladder.  The 
bladder  in  consequence  becomes  gradually  more  dis- 
tended and  the  residual  urine  steadily  increases.  The 
chronic  over-distention  mechanically  impairs  the  blood 


KESULTS  OF  SYPHILITIC  LESIONS        133 

supply  of  the  bladder  muscles,  and  the  overstretched, 
ill-nourished  muscles  weaken.  The  muscles  of  the  blad- 
der wall  may  also  sometimes  weaken  because  of  the 
involvement  of  the  nerve  fibers  of  their  tone  reflex  in  a 
tabetic  lesion. 

The  unperceived  excess  of  urine  in  the  anesthetic 
and  muscularly  weak  bladder  may  mechanically  force 
the  stretched,  weakened  sphincter,  especially  during 
coughing,  or  sneezing,  or  lifting,  or  bending,  or  other 
circumstances  in  which  the  intra-abdominal  pressure  is 
suddenly  raised.  A  few  drops  of  urine  escape  along  the 
insensitive  urethra  and  the  patient  is  astonished  to  feel 
the  unexpected  wetness  on  his  thighs.  Often  the  initial, 
and  sometimes  the  only,  accident  of  this  kind  occurs,  not 
during  exertion,  but  during  the  sphincter  relaxation  of 
sleep.  These  accidents  increase  in  frequency.  The 
urine-soaked  garments  of  the  tabetic  are  an  unpleasant 
feature  of  most  neurological  clinics. 

The  weakness  of  the  expelling  power  renders  micturi- 
tion not  only  an  incomplete  but  a  lengthy  process.  The 
stream  has  not  force  adequately  to  distend  the  urethral 
walls,  so  it  issues  small,  may  be  forked;  and,  instead 
of  continuing  powerfully  forward,  falls  immediately  from 
the  urinary  orifice.  Indeed,  there  may  be  no  stream, 
merely  a  discontinuous  trickle,  which  the  tabetic  must 
direct  away  from  his  person. 

The  tabetic  may  lose  all  desire  and  urinate  only  from 
a  sense  of  expediency  or  from  the  wish  to  evade  drib- 
bling. The  act  is  then  performed  in  complete  isolation ; 
he  sits  or  kneels  or  bends,  presses  on  his  abdomen, 
coughs  and  evokes  the  aid  of  the  sound  of  running  water. 
Sometimes,  he  can  urinate  only  if  immersed  in  a  bath. 
And  when  thinking  the  act  complete,  he  adjusts  his 


134  LOCOMOTOR  ATAXIA 

garments,  he  may  be  annoyed  by  continued  dribbling. 
Immediately  after  urination,  the  tabetic  bladder  may 
yield  five  or  more  ounces  to  a  catheter. 

The  intermittent  trickle  of  urine  in  tabes  is  not  like 
the  flow  from  a  fistula ;  nor  is  it  a  paralytic  incontinence. 
It  is  purely  a  mechanical  effect  analogous  to  the  over- 
flow which  occurs  from  a  bladder  with  an  enlarged 
prostate.  There  is  no  leakage  in  tabes  unless  the  bulk 
of  the  urine  exceeds  the  containing  power  of  the  bladder : 
dribbling  in  tabes  results  solely  from  over-distention, 
the  product  of  infrequent  and  imperfect  emptying.  If, 
by  periodic  evacuation,  the  bladder  be  prevented  from 
over  distending,  the  muscle  gradually  recovers  much  of 
its  tone  and  the  dribbling  stops. 

Neglect  may  lead  to  fatal  cystitis. 


CHAPTER  VII 

RESULTS  OF  THE  SYPHILITIC  LESIONS  OF  THE  VEGETA- 
TIVE NERVOUS  SYSTEM 

b.  DISTURBANCES  OF  CHEMICAL  CORRELATION 

Action  of  the  products  of  the  internal  secreting  glands.  The  antago- 
nistic reaction  to  chemical  substances  shown  by  the  vagal  and  the 
sympathetic  components  of  the  vegetative  nervous  system.  Oscil- 
lations in  the  balance  between  vagal  and  sympathetic  components, 
due  to  chemical  stimuli,  control  metabolism,  and  defense  against 
organismal  invasion.  Disturbance  of  this  control.  Trophic  con- 
ditions: ulcers,  infections,  fractures,  arthropathies.  Defense 
against  the  spirochete.  Production  of  defense  substances.  Stimu- 
lation of  vegetative  nervous  system  by  defense  substances.  Ade- 
quate stimulation  causing  perfect  defense;  inadequate  stimulation 
permitting  persistence  of  the  spirochete.  Inadequate  stimulation 
due  to  mildness  of  pretabetic  lesions:  to  glandular  insufficiency : 
to  age :  to  mental  stress.  Imperfect  defense ;  causes.  Effect  of 
lesions  of  vegetative  nervous  system  upon  defense.  Why  optic 
tabes  is  abortive.  Why  the  vegetative  nervous  system,  although 
the  first,  is  not,  as  a  rule,  the  main  site  of  spirochete  invasion. 

IN  the  body  cellular  masses  occur  called  internal 
secreting  or  endocrinous  glands.  These  cells  produce 
chemical  substances  commonly  but,  as  a  rule,  incorrectly 
called  hormones,  that  are  poured  into  the  blood  and 
conveyed  by  it  throughout  the  body.  Our  knowledge  of 
hormones  is  slight.  The  hormone  of  one  endocrinous 
gland  is  said  to  excite  the  secretory  activity  of  another, 
or  inhibit  that  of  a  third.  A  hormone  is  supposed  to 
reinforce  or  to  antagonize,  completely,  or  in  part,  the 
activity  of  another  hormone.  These  "hormones,  by  their 
direct  action,  modify  the  biochemical  processes  of  all 
tissue  cells,  mainly  in  the  course  of  a  slow  general  diffu- 

135 


136  LOCOMOTOR  ATAXTA 

sion  by  the  blood  and  lymph,  but  partly  by  stimulating 
the  receptors  of  the  vegetative  nervous  system. 

The  sympathetic  and  the  vagal  (autonomic)  com- 
ponents of  the  vegetative  nervous  system  show  towards 
one  hormone,  adrenalin,  and  towards  other  chemical  sub- 
stances antagonistic  reactions. 

Adrenalin,  the  hormone  of  the  suprarenal  gland,  stim- 

ulates the  sympathetic;  the  resulting  increase  of  irri- 

Para'ysis  tability,  or  tone, 

Atropin  y' 

i    ^^^-"         in    the    sympa- 

F^"-""^  _       thetic  is   accom- 


~~~  .  __  ^7\ 

^--^     L\  panied   by    dim-. 

s'O^T  J  inution    of   tone 

Adrenalin 

in  the  vagal  com- 

Stimulation 

FIG.  56.—  Diagram  of  autonomic  or  vagal  (V,  V1)  ponent,  and,  ill 
and  sympathetic  (S,  S1)  interaction.  SFV  consequence  by 
represents  the  balancing  of  vagal  action  by  sym- 

pathetic.  S1  F  V1  shows  the  effect  of  stimulating  decreased  actlV- 
the  sympathetic  by  adrenalin  or  of  paralysing  j^y  jj^  the  Dan- 
the  autonomic  with  atropin. 

creas  and  in  the 

thyroid  glands.  Cholin  produces  increase  of  tone  in 
the  vagus  with  concomitant  diminution  of  tone  in  the 
sympathetic.  Most  of  the  manifestations  of  anaphylaxis 
are  attributable  to  increased  vagal  irritability.  The  in- 
creased vagal  tone  may  be  counteracted  by  paralyzing 
the  vagus  with  atropin  or  by  stimulating  the  sympathetic 
with  adrenalin.  Oscillations  in  the  balance  of  tone  be- 
tween these  two  antagonistic  components  of  the  vegeta- 
tive nervous  system,  brought  about  by  chemical  stimuli, 
control  metabolism,  and  the  kindred  function  of  defense 
against  organismal  invasion. 

The  cellular  confederacy,  which  we  call  the  human 
body,  may  be  disturbed  locally  by  the  implication  of  the 
vegetative  reflex  arcs  in  the  tabetic  process,  and  generally 


RESULTS  OF  SYPHILITIC  LESIONS        137 


by  the  destroying  of  the  balance  of  tone  between  the 
vagus  and  the  sympathetic:  then,  cellular  activity  does 
not  correspond  to  the  needs  of  the  body.    Thus,  pressure 
normally  tolerated  with  impunity  on  the  sole  of  the  foot 
may  give  rise  to  ulcers;  trophic  changes  may  appear  in 
the  toe  nails  and  skin;  in- 
fections may   readily   oc- 
cur around  the  nail  bed, 
and  the  bones  may  become 
so  brittle  that  they  frac- 
ture even  from  the  feeble 
strain  of  their  weakly  con- 
tracting   muscles.      Such 
fractures   may   be   multi- 
ple. The  tendency  to  frac- 
ture is  said  to  be  lessened 
by  administration  of  the 
thyroid    and   parathyroid 
glands.     I   once   saw   the 
bones  of  the  leg  markedly 
atrophy.     As  a  corollary 
to  this  rarefaction  of  the 
bones,  an  overgrowth  l  oc- 
casionally    occurs.       The 
bony  overgrowth  is  pain- 
less and  develops  at  any 
stage  of  the  disease.     It  is  often  a   sequel  to  injury. 
Touch  may  reveal,  especially  in  cases  with  effusion,  a 
higher  temperature  over  the  affected  joint  than  over  its 

1  Its  cause  has  occasioned  prolonged  controversy.  Stargardt  sees  in 
it  an  osteitis  analogous  to  syphilitic  inflammation  elsewhere.  Most 
believe  that  the  proliferation  is  comparable  with  that  which  occurs  in 
syringomyelia,  and  that  it  is  wholly  due  to  the  nervous  lesions  of 
tabes. 


FIG.  57. — Trophic  ulcer  on  the  plantar 
aspect  of  the  big  toe  of  a  tabetic. 
The  prehensile  attitude  of  these 
toes  was  habitual. 


138 


LOCOMOTOR  ATAXIA 


unaltered  fellow.  When  the  arthropathy  attacks  the  tar- 
sometatarsal  joints,  perforating  ulcers  may  be  associated 
with  it.  Arthropathy  may  reinforce  hypotonia  in  pro- 
ducing dislocations. 

As  the  syphilitic  infection  early  becomes  general,  the 
, . .  order  in  which  the  tis- 
sues are  attacked  must 
be  the  order  of  their  vul- 
nerability. The  lateness 
of  nervous  lesions  in 
syphilis  implies  there- 
fore that  the  tissues  of 
the  central  nervous  sys- 
tem possess  a  resistance 
to  invasion  by  ordinary 
strains  of  spirochete 
greater  than  the  resist- 
ance of  tissues  which  are 
earlier  invaded.  No- 
guchi  and  Reasoner  have 
emphasized  this  resist- 
ance of  nerve  tissues. 
But  Noguchi  (P  r  e  s  s  e 
medicate,  1913,  viii,  1905) 
has  done  more.  He  has 
shown  that  the  nervous 
system  of  rabbits  which 
have  been  frequently  inoculated  intravenously  with 
spirochetes  throughout  a  period  of  five  months,  loses  this 
refractory  tendency;  that  repeated  intravenous  infec- 
tions sensitize  the  nervous  tissues  to  spirochete  invasion. 
In  other  words  the  body's  reaction  to  the  spirochete  is 
not  a  local  but  a  general  biochemical  response.  This  gen- 


Fia.  58. — Trophic   ulcer   on   the   outer 
margin  of  the  foot  of  a  tabetic. 


RESULTS  OF  SYPHILITIC  LESIONS        139 

eral  alteration  in  the  cellular  response  was  further  dem- 
onstrated by  the  experiments  of  Finger  and  Landsteiner : 
these  observers  were  able  in  human  beings  suffering  from 
secondary  syphilis  to  induce  by  spirochete  inoculation 
only  secondary  lesions ;  and  in  others  suffering  from  ter- 
tiary syphilis,  only  tertiary  lesions.  Krafft-Ebbing 
failed  to  produce  any  lesions  in  non-nervous  tissues  by 


FIG.  59. — Taboparesis.      Bed  sores  over  heels,  sacrum,  buttocks,  back  and 

sides.     (Jelliffe.) 

inoculating    subcutaneously    a    series    of   nine    general 
paretics,  with  scrapings  from  primary  sores. 

In  a  person  infected  with  syphilis,  when  the  tissue  first 
invaded  finally  heals,  the  spirochete  next  grows,  not  in  it, 
but  in  other  tissues.  The  cells  of  the  first  attacked  tissue 
in  repelling  the  invasion  acquire  power  to  resist  the  spiro- 
chete and  acquire  an  immunity  to  the  invasion  greater 
than  that  which  other  tissues  now  enjoy.  This  has  long 
been  known  from  clinical  observation,  and  has  also  been 
experimentally  demonstrated.  Thus,  Truffi,  P.  Ullmann 
and  Tomasczewski  report  that  in  dogs  a  second  syphil- 


140 


LOCOMOTOR  ATAXIA 


itic  infection,  seven  to  nine  weeks  after  a  first,  may  be 
entirely  without  visible  effect.  There  is,  however,  usually 
some  reaction,  so  these  observers  conclude  that  the 
immunity  acquired  by  the  tissue  in  its  defense  against 


FIG.  60. — Painless  tabetic  fracture  of 
the  head  of  the  tibia. 


FIG.  61. — Charcot  left  knee  and 
ankle  with  trophic  changes  in 
the  toes. 


the  first  injection  is,  as  a  rule,  not  absolute.  Perhaps 
the  amount  of  reaction  which  the  second  injection  evokes 
is  partly  an  index,  not  of  failure  of  the  tissues  to  acquire 
complete  immunity  to  the  first,  but  of  the  biological  dif- 
ference between  the  spirochete  of  the  second  injection 
and  that  of  the  first. 


B 

FIG.  62. — Tabetic  joints:    A,  Charcot  right  wrist;  B,  its  x-ray. 

141 


142  LOCOMOTOR  ATAXIA 

Tomasczewski  and  his  fellow-workers  showed  that  im- 
munizing the  eye  bestowed  no  detectable  immunity  on 
the  skin.  The  careful  seeking  of  competent  observers 
has  failed  to  reveal  the  presence  of  defense  substances. 


FIG.  63. — Charcot  elbow.    This  tabetic  also  had  wasting  of  the  muscles  of 

the  left  thumb. 

Such  failure  may  imply  merely  faulty  methods  of  search. 
Ehrlich  states  that  substances  which  activate  salvarsan 
are  present  in  the  blood  and  absent  from  the  cerebro- 
spinal  fluid.  Syphilitic  lesions  occur  in  crops  separated 
by  periods  of  outwardly  perfect  quiescence;  the  begin- 
ning of  such  a  period  synchronizes  with  the  healing  of 


Fig.  64 


Fig.  65 

FIGS.  64  and  65. — Proliferating  osteitis  of  lower  left  ribs  in  a  tabetic.  (Jelliffe.) 

143 


144  LOCOMOTOK  ATAXIA 

the  lesions,  with  the  destruction  of  the  spirochete;  the 
end  of  the  period  with  renewed  growth  of  the  spirochete, 
with  fresh  lesions ;  similar  but  longer  periods  may  occur 
between  successive  invasions  of  different  types  of  tis- 
sues, and  before  the  first  nervous  symptom  appears, 


v        •»  * 


v 

\«    . 


•*» 

"•*'-         -  *"        '  *  ' 


I 


u 


FIG.  66.— Experimental  brain  syphilis  produced  in  a  rabbit  by  sensitising 
through  repeated  inoculation  with  the  Spirochaeta  pallida.     (Noguchi.) 


EESULTS  OF  SYPHILITIC  LESIONS        145 

years  may  elapse.  A  single  injection  or  a  few  crops  of 
lesions  of  inconsiderable  extent  may  immunize  a  whole 
tissue. 

After  a  staphylococcal  infection,  a  guinea  pig  immun- 
ized against  many  thousand  minimal  lethal  doses  of 
tetanus  was  observed  by  Roux  to  succumb  to  one:  a 
dissociation  of  the  loose  innocuous  chemical  combination 
between  the  tetanic  toxin  and  antitoxin  occurred  owing 
to  the  staphylococcal  infection.  Chills  and  bacterial  in- 
fection may  be  followed  either  by  the  onset  of  tabes,  or, 
in  tabes,  by  marked  progress  in  the  lesions. 

The  quiescent  periods  between  the  lesions,  the  influence 
of  time  in  decreasing  the  resistance,  the  immunizing  of 
whole  tissues  from  points  of  successful  defense  in  them, 
and  the  effect  of  intercurrent  infections,  show  that  in 
syphilis  defensive  substances  are  produced.  These  de- 
fensive substances  issue  not  only  from  invaded  cells 
but  also  from  cells  not  immediately  menaced,  which  are 
stimulated  to  resist  by  products  derived  from  attacked 
cells  and  from  the  spirochete.  There  is  a  concerted  and 
correlated  response  of  the  tissue  cells  to  the  chemical 
substances  which  arise  during  spirochete  invasion. 

In  the  normal  course  of  spirochete  invasion,  owing  to 
successive  immunization  of  the  skin,  mucous  membranes 
and  deeper  tissues,  a  general  defensive  response  is 
engendered  which  causes  the  final  quiescence  of  the 
spirochete,  or  makes  the  uninvaded  tissues  immune. 
Lack  of  the  normal  chemical  stimulation,  due  either  to 
absence  or  to  inadequacy  of  the  local  defense  reactions 
in  the  skin,  mucous  membranes  and  deeper  tissues,  may 
prevent  the  proper  excitation  of  the  vegetative  system 
and  may  thus  prevent  the  perfect  correlation  of  the 
chemical  confederacy  which  is  necessary  to  ensure  de- 


146  LOCOMOTOR  ATAXIA 

fense  of  nerve  tissues  against  the  spiroehete.  The 
occurrence  of  tabes  after  no  or  mild  pretabetic  lesions 
may  be  due  in  part  to  the  insignificance  of  these  lesions. 

In  the  aged  the  activity  of  the  endocrinous  glands 
diminishes:  Pitres  has  emphasized  the  rapid  course  of 
senile  tabes.  Joffroy,  Oppenheim,  Pierre  Marie  and 
others  have  noted  the  association  of  tabes  with  disease 
of  the  thyroid  gland.  Oppenheim  has  emphasized  the 
value  of  pituitary  extract  in  tabes.  The  fulminating 
spread  of  tabetic  lesions  which  occasionally  follows  sal- 
varsan  injections  is  said  to  be  obviated  by  the  use  of 
adrenalin. 

The  average  age  of  onset  of  tabes  is  approximately  37 
years.  About  this  age  most  acquired  insanities  begin; 
carcinomata  usually  appear.  It  is  the  average  limit  of 
endurance,  the  age  when  the  balance  of  mental  and  of 
vegetative  life  fails,  owing  to  the  stress  of  living. 

The  tabetic  often  volunteers  the  statement  that  his 
symptoms  are  due  to  prolonged  worry.  He  may  be 
able  even  to  prove  that  they  commenced  soon  after  a 
shock  he  experienced.  Tabes  so  frequently  follows  an 
accident  that  Hitzig  incurred  ridicule  by  teaching  that 
accidents  liberate  toxins  which  lead  to  tabes.  The  physi- 
cal accident  to  which  tabes  is  attributed  is  seldom  severe. 
Minop  of  Moscow  showed  that  slight  lacerations  of  the 
lymph  and  vascular  capillaries  of  the  cord  occur  after 
severe  accidents  to  the  spinal  column,  which  have  not 
destroyed  the  continuity  of  the  cord.  But  such  changes 
are  not  confined  to  the  root  zones  nor  to  the  dorsal 
columns.  Such  changes  cannot  produce  only  the  signs 
which  are  discovered  in  cases  of  tabes  attributed  to 
accident.  The  importance  of  the  injury,  as  a  factor  in 
causing  tabes,  lies  not  so  much  in  the  immediate  physical 


EESULTS  OF  SYPHILITIC  LESIONS        147 

consequences  as  in  the  mental  effect  of  the  shock  and  the 
pain. 

The  ratio  of  tabes  to  syphilis  is  higher  among  Euro- 
peans than  among  Chinese,  Persians,  Egyptians,  and 
negroes ;  among  men  than  among  women ;  and  among  the 
intellectual  than  among  the  laboring  classes.  In  the 
French  and  Austrian  armies  painstaking  statistical  in- 
quiries have  shown  that  the  ratio  of  tabes  to  syphilis  is 
remarkably  higher  among  the  officers  than  among  the 
men. 

The  races  in  which  tabes  is  rare,  in  which  the  resist- 
ance to  the  spirochete  is  not  imperfect,  enjoy  in  common 
a  placid  existence,  apart  from  the  strife  and  turmoil  of 
our  civilization;  an  interesting  corollary  is  found  in  the 
United  States,  where  the  negro  yearly  enters  more  and 
more  into  the  competition  of  modern  life,  and  yearly 
loses  more  of  his  freedom  'from  tabes;  indeed,  a  case 
of  tabes  in  a  negro  there,  once  .noteworthy,  is  now  com- 
monplace. The  occurrence  of  tabes  mainly  among  males 
and  mainly  among  the  intellectual  .classes  also  suggests 
that  the  mental  stress  of  a  modern  environment  or  of 
an  intellectual  occupation  may  predispose  the  syphilitic 
to  tabes. 

We  have  already  mentioned  (p.  119)  the  presence  of 
cell  groups  in  the  central  nervous  system,  which  are 
called  centers  of  vegetative  function.  These  centers  cor- 
relate vegetative  processes  in  response  not  merely  to 
peripheral  but  also  to  psychic  demands.  For  every 
psychic  process  there  is  a  concomitant  physicochemical 
equivalent.  These  equivalents  are  unconsciously  evoked ; 
thus,  with  shame  occurs  blushing,  dilatation  of  the  blood 
vessels  of  the  face  and  neck;  with  fear,  pallor — vaso- 
constriction — accelerated  heart  action,  goose  flesh  and 


148  LOCOMOTOR  ATAXIA 

relaxation  of  sphincters;  and  with  intellectual  effort  a 
rise  of  blood  pressure. 

The  rise  in  blood  pressure  during  mental  effort  has 
been  shown  by  Cannon  and  de  la  Paz  to  be  accompanied 
by  increased  secretion  in  the  adrenal  glands.  Cannon 
also  has  shown  that  in  states  of  fear  there  is  an  augmen- 
tation in  the  amount  of  adrenalin  in  the  blood. 

The  more  frequent  the  rise  of  blood  pressure  due  to 
psychic  effort,  the  longer  the  pressure  takes  to  resume 
the  normal  average  in  the  resting  intervals;  the  more 
does  this  resting  average  tend  to  rise ;  and  the  more  do 
excessive  rises  result  from  mental  effort.  In  other 
words,  the  more  frequent  or  the  more  prolonged  the 
mental  effort,  the  more  irritable  is  the  sympathetic,  the 
more  is  its  normal  balance  with  the  vagus  disturbed. 

In  syphilitics  exposed  to  mental  strain,  slow  and  ir- 
regular heart  action ;  nausea,  hypersecretion  and  abnor- 
mal gastric  movements;  spastic  constipation;  and  other 
symptoms  characteristic  of  unbalanced  vagal  irritability 
occur.  To  test  the  vagal  tone,  clinicians  inject  O.Olgm., 
of  pilocarpin  hydrochlorid.  An  abnormal  degree  of 
sweating  and  salivation  shows  the  presence  of  vagal 
irritability.  Not  only  may  vagotonia  be  thus  revealed  in 
syphilis,  but  a  gastric  crisis  may  sometimes  be  evoked, 
disclosing  the  presence  of  unsuspected  incipient  tabes 
(Hess  and  Eppinger). 

Intellectual  strain  disorganizes  the  normal  balance  of 
tone  between  the  antagonistic  vagal  and  sympathetic 
components  of  the  vegetative  system;  impairs  in  conse- 
quence that  regulation  by  the  vegetative  nervous  system 
of  the  chemical  confederacy  which  ensures  the  defense 
of  the  body  against  spirochete  invasion;  and,  therefore, 
renders  the  defense  imperfect.  In  consequence  the  spiro- 


EESULTS  OF  SYPHILITIC  LESIONS        149 

chete  persists  to  cause  tabes.  A  virulent  infection  may 
bring  tabes  to  the  normal  individual,  but  an  infection 
of  average  virulence  will  bring  it  to  the  nervous.  The 
nervous  syphilitic  is  a  potential  tabetic,  a  potential 
general  paretic.  The  liability  of  the  tabetic  to  pneu- 
monia, tuberculosis  and  other  intercurrent  infections, 
may  be  due  in  part  to  his  disease;  but  it  is  due  in  part, 
also,  to  the  imperfect  defense  to  which  the  occurrence 
of  tabes  is  attributable. 

The  imperfection  of  the  tabetic's  defense  against  the 
spirochete  may  be  inherited;  nervous  lesions  have  been 
reported  in  members  of  the  same  family  who  were  in- 
fected with  syphilis  from  separate  sources:  it  may  be 
acquired  owing  to  environmental  or  occupational  condi- 
tions causing  mental  stress  which  disturbs  the  normal 
balance  of  the  vegetative  system;  it  may  be  due  to  the 
mildness  or  absence  of  the  pretabetic  lesions  causing  an 
inadequate  production  of  defense  substances,  an  inade- 
quacy in  the  chemical  stimulation  of  the  vegetative 
nervous  system ;  it  may  be  due  to  the  invincible  virulence 
of  the  attacking  spirochete.  This  imperfect  defense 
enables  the  spirochete  to  persist  active.  The  attacking 
force  of  the  spirochetes,  their  number  and  their  virulence, 
depends  not  merely  upon  qualities  inherent  to  the  spiro- 
chete, but  also  upon  the  efficiency  of  the  defenses  outside 
of  the  central  nervous  system.  Cases  with  lesions  of  the 
vegetative,  nervous  system,  which  controls  this  defense, 
are,  ipso  facto,  exposed  to  a  greater  attacking  force  than 
cases  in  which  this  controlling  mechanism  escapes. 

In  optic  tabes  the  vegetative  nervous  system  is  seldom 
widely  implicated ;  the  central  nervous  system  may  thus 
confront  only  a  few  persistent  spirochetes:  whereas  in 
spinal  tabes  not  only  may  the  vagal  component  be  found 


150  LOCOMOTOR  ATAXIA 

extensively  degenerated,  but  the  sympathetic  fibers  in 
the  posterior  roots  are  invariably  attacked.  A  more  or 
less  continuous  stream  of  spirochetes  may  be  liberated 
from  a  quiescent  resistant  stage  by  the  gradual  deteriora- 
tion which  the  general  defense  undergoes,  as  the  control 
of  the  vegetative  nervous  system  fails.  The  insignifi- 
cance of  the  vegetative  lesions  and  in  optic  tabes  may  be 
a  factor  in  making  that  form  the  abortive  form  of  tabes, 
the  "forme  fruste  par  excellence"  (Fournier). 

As  tabes  beginning  in  the  posterior  roots  affects, 
mainly  posterior  roots;  as  tabes  beginning  in  one  optic 
nerve  next  affects  the  other;  and  as  the  resulting  optic 
degeneration  is  greater  when  tabes  begins  in  the  optic 
nerve  than  when  optic  atrophy  follows  spinal  atrophy, 
the  spirochete  seems  to  grow  best  in  sites  which  are 
chemically  similar  to  that  where  it  first  grows  in  the 
central  nervous  system.  The  usual  site  first  attacked  in 
the  central  nervous  system  is,  however,  neither  the  pos- 
terior roots  nor  the  optic  nerve,  but  that  part  of  the 
vegetative  nervous  system  which  supplies  the  pupil. 
Sometimes  the  disease  spreads  mainly  in  the  vegetative 
nervous  system:  many  cases  of  tabes  complain  first  of 
bladder  symptoms;  some  tabetics  are  troubled  almost 
exclusively  with  gastric  crises.  But,  usually,  after  affect- 
ing the  vegetative  nervous  system  of  the  pupil,  posterior 
root  lesions  occur.  The  vegetative  nervous  system 
responds  to  chemical  stimuli.  Different  chemical  stimuli 
affect  different  parts  of  the  system.  There  is,  therefore, 
probably  a  lack  of  uniformity  in  the  chemical  composi- 
tion of  the  several  parts  of  the  vegetative  nervous 
system,  a  lack  which  may  explain  why  the  vegetative 
nervous  system,  although  the  first  site,  is  not,  as  a  rule, 
the  main  site  of  the  spirochete 's  invasion. 


CHAPTER  VIII 

DIAGNOSIS  AND  COURSE  OF  TABES 

Symptoms  and  signs  of  tabes.  Their  origin.  Diagnosis  of  syphilis. 
First  sign  of  invasion  of  nervous  system.  Course  of  invasion  be- 
ginning in  posterior  root;  beginning  in  optic  nerve.  Tabes  diag- 
nosed by  evolution.  Tabes  a  disease  in  which  dominant  symptoms 
arise  from  primary  syphilitic  invasion  of  posterior  nerve  roots. 
Pretabetic  period,  duration,  and  significance.  Effect  of  age  on 
pretabetic  period.  Rate  of  syphilitic  invasion.  Rapid,  slow  and 
abortive  invasions.  Remissions.  Preataxic  stage.  Ataxic  stage. 
"Paralytic"  or  surrender  stage.  These  stages  psychological,  not 
anatomical.  Types  of  tabes.  Age  of  onset  of  tabes.  Termination 
of  tabes. 

THE  observers  named  in  the  following  table  record  the 
frequency  of  the  signs  and  symptoms  (Abadie  signs 
only)  which  they  have  observed  in  tabes,  as  follows : 

Schaffer 

Leimbach  200  cases 

400  eases    Abadie     Sarbo    Incipient  Advanced 

Absent  knee-jerks 96.52%  70%  89.40% 

Absent  Achilles  jerks 82  91.00  14%  71.6% 

Romberg's  sign 88.75  ..  93.00  25  73.3 

Lightning  pains 88.25  . .  93.00  53  90. 

Bladder  trouble 65  79.00  14  63.3 

Pupillary  disturbances 65  88.80  89  98.3 

Peroneal  anesthesia 80  88.50 

Ulnar  anesthesia    . .  66.00  

Of  these,  we  have  shown  the  pupillary,  the  bladder, 
and,  in  part,  the  lightning  pains  to  be  due  to  implication 
of  the  vegetative  nervous  system;  the  loss  of  tendon 
reflexes  and  the  common  sensory  loss  to  be  due  to  im- 
plication of  sensory  fibers  in  the  posterior  nerve  roots; 

151 


152  LOCOMOTOR  ATAXIA 

and  Romberg's  sign  to  be  due  partly  to  sensory  loss  and 
partly  to  mental  causes. 

The  vegetative,  non-vegetative,  sentient,  and  non-sen- 
tient fibers  of  the  afferent  nervous  mechanism  are  thus 
implicated  in  the  syphilitic  invasion  of  the  nervous  sys- 
tem styled  tabes.  Its  diagnosis  rests  upon  evidence  of 
syphilis  and  evidence  of  implication  of  the  afferent 
nervous  mechanism. 

In  all  reactions  of  the  tissues  to  organisms,  in  all 
inflammations,  organismal  toxins  produce  by  chemotaxis 
a  serous  and  a  cellular  exudate  at  the  site  of  invasion. 
The  tissue  reaction  to  the  spirochete  in  the  central 
nervous  system  increases  the  bulk  arid  the  content  of  the 
cerebrospinal  fluid.  The  increase  of  the  bulk  of  the 
cerebrospinal  fluid  causes  a  raising  of  its  pressure, 
which  is  evident  in  the  greater  force  of  its  flow  when 
the  fluid  is  tapped  by  lumbar  puncture.  The  increase 
in  the  contents  consists  mainly  of  globulin  and  of  small 
lymphocytes.  The  amount  of  globulin  varies.  Apelt  and 
Nonne,  by  careful  investigations,  have  determined  the 
amounts  of  globulin  which  commonly  occur  in  tabes  and 
have  stated  that  the  probability  of  the  presence  of  tabes 
may  be  gauged  from  these  amounts.  The  occasional  cell 
seen  normally  in  a  microscope  field  of  the  centrifugalized 
cerebrospinal  fluid  is  multiplied  twenty  to  sixty  fold  in 
tabes.  But  more  important  than  these  inflammatory  evi- 
dences is  the  presence  in  the  cerebrospinal  fluid  of  the 
substance  which  is  practically  pathognomonic  of  syphilis, 
the  Wassermann  substance.  From  the  globulin  content, 
the  cell  count,  and  the  Wassermann  reaction  in  the 
cerebrospinal  fluid,  the  presence  or  absence  of  the  spiro- 
chete in  the  central  nervous  system  is  presumed  (see 
Warthin's  researches,  p.  170). 


DIAGNOSIS  AND  COURSE  OF  TABES       153 

Mental  stress  is  often  a  causal  factor  in  bringing  tabes 
to  the  syphilitic.  The  earliest  symptom  of  syphilitic 
invasion  of  the  nervous  system  may  be  neurasthenia. 
The  future  course  of  the  syphilitic  neurasthenic  cannot 
be  foretold.  He  may  develop  no  further  symptoms  or 
he  may  become  a  paretic  or  a  tabetic.  In  testing  with 
atropin  the  vagal  irritability  of  a  syphilitic  neurasthenic, 
Hess  and  Eppinger  elicited  a  gastric  crisis  and  discov- 
ered the  presence  of  unsuspected  tabes. 

The  earliest  sign  of  syphilitic  invasion  of  the  central 
nervous  system  is  the  Argyll-Robertson  pupil  or  its  pre- 
cursors. But  variation  in  the  shape  or  the  size  of  the 
pupil  or  diminution  of  its  contractility  to  light,  is  by 
none  alleged  to  suffice  for  a  diagnosis  of  tabes.  An 
Argyll-Robertson  pupil  may  be  followed  by  tabes,  by 
paresis,  by  optic  atrophy,  by  amyotrophic  lateral  scle- 
rosis, by  any  of  the  groups  of  symptoms  which  may  fol- 
low syphilitic  invasion  of  the  central  nervous  system.  It 
may  also  be  the  unique  sign  of  an  abortive  invasion. 

There  is  no  agreement  regarding  the  minimum  that 
constitutes  tabes.  Lightning  pains  we  have  seen  are 
due  to  irritation  of  the  vegetative  or  of  the  common 
pain  fibers  usually  in  the  posterior  root.  Root  irritation 
may  be  caused  by  inflammatory  processes,  or  by  the 
pressure  of  a  tumor  or  of  an  aneurysm.  In  a  syphilitic, 
such  pains  occurring  without  evidence  of  root  pressure 
usually  arouse  the  first  suspicion  of  tabes.  Less  than 
pupillary  changes  and  lightning  pains  seldom  suggest 
tabes.  The  first  suspicion  of  tabes  arises,  therefore, 
from  a  syphilitic  implication  of  the  vegetative  and  the 
sensory  systems.  The  single  site  at  which  such  implica- 
tion commonly  occurs  is  the  posterior  root.  Hence  the 
possibility  of  tabes  suggested  by  pupillary  changes  and 


154  LOCOMOTOR  ATAXIA 

lightning  pains  becomes  a  probability  when  there  occurs 
also  a  loss  of  tendon  reflexes  due  neither  to  alcohol,  nor 
to  diabetes,  and  not  associated  with  pain  on  pressure  such 
as  is  seen  in  neuritis.  If  to  this  loss  be  added  a  loss  of 
sensibility  to  pain  greater  in  area  than  that  of  the  loss 
to  touch,  the  existence  of  a  posterior  root  lesion  becomes 
certain. 

We  have  seen  that  with  the  exception  of  the  vegetative 
system,  the  site  first  attacked  is  usually  the  chief  site 
of  the  invasion,  that  syphilitic  invasion  beginning  in  the 
optic  nerve  affects  it  mainly;  that  when  the  invasion 
begins  in  the  optic  nerve,  the  destruction  there  is  usually 
more  severe  than  when  optic  follows  posterior  root  in- 
vasion; that  invasion  beginning  in  the  optic  nerve  may 
be  confined  there,  whereas  invasion  beginning  in  the 
posterior  root,  although  affecting  mainly  posterior  roots, 
may  later  implicate  any  cranial  nerve  and  may  become 
almost  coextensive  with  the  central  nervous  system.  A 
primary  optic  lesion  is  thus  associated  with  a  more  or 
less  characteristic  invasion;  so  also  is  the  primary  pos- 
terior root  lesion. 

We  have  seen  that  the  vegetative  nervous  system 
controls  the  chemical  confederacy  to  which  defense 
against  organismal  invasion  is  entrusted.  Lesions  of 
that  system  may  permit  weakly  spirochetes  to  persist, 
may  allow  inactive  spirochetes  to  become  aggressive, 
may  entail  successive  streams  of  organisms  sensitizing 
and  later  invading  the  nervous  system.  Posterior  root 
lesions  imply  vegetative  lesions.  Optic  nerve  lesions  do 
not.  Hence  the  initial  site  of  the  invasion  somewhat 
presages  the  course. 

The  syphilitic  posterior  root  lesion  does  not  make  the 
presence  of  tabes  certain.  Paresis  remains  paresis  in 


spite  of  root  lesions.  Syphilitic  root  lesions  in  aortic 
disease  are  not  considered  as  tabetic.  Root  lesions  may 
occur  in  cerebral  gummata.  It  is  recognition  that  the 
source  of  the  dominant  symptoms  is  primary  syphilitic 
invasion  of  the  posterior  roots  which  leads  to  a  diagnosis 
of  tabes.  When  symptoms  are  few,  we  wait  till  the 
certainty  of  a  posterior  root  lesion  can  be  established. 
When  symptoms  are  many,  we  ignore  the  posterior  root 
lesion  if,  as  in  paresis,  it  does  not  dominate  the  disease 
picture.  It  is  the  course,  not  the  site,  of  the  invasion 
which  we  strive  consciously  or  unconsciously  to  deter- 
mine. We  diagnose  syphilitic  invasions  by  evolution. 

Regarding  the  diagnosis  of  "1'ataxie  locomotrice 
progressive, ' '  Duchenne  states : — 

"What  really  makes  the  ataxia  a  distinct,  morbid  entity,  is 
the  regularity  in  general  of  its  mode  of  appearance  and  of  the 
development  of  the  symptoms;  it  is  their  sequence,  in  other 
words,  their  order.  Ataxia  can  be. divided  into  three  distinct 
periods ;  the  first  characterised  by  the  paralysis  of  one  or  several 
motor  nerves  of  the  eye  complicated  by  the  paralysis  of  the 
optic  nerve  and  by  pains,  shooting,  erratic;  the  second,  by  the 
appearance  of  troubles  of  coordination  usually  in  the  lower  limbs 
but  sometimes  in  the  upper;  the  third,  by  the  generalization  of 
the  malady." 

There  is  no  pathognomonic  sign  of  tabes.  We  must 
still,  like  Duchenne,  base  the  diagnosis  upon  evolution. 
But  the  discovery  by  Argyll-Robertson  of  Edinburgh 
(1869)  of  the  loss  of  light  reaction  in  the  pupil  of 
syphilis;  by  Westphal  (1875)  of  the  loss  of  the  knee- 
jerks;  by  Erb  of  the  swaying  when  the  tabetic  stands 
with  closed  eyes  (Romberg's  sign);  by  Wassermann  of 
the  serological  evidence  of  syphilis;  and  by  Head  and 
Sherren  of  the  nature  of  the  sensory  loss  in  root  lesions, 


156  LOCOMOTOR  ATAXIA 

enables  us  to  recognize  tabes  without  waiting  so  long 
as  Duchenne. 

The  period  between  the  causal  syphilitic  infection  and 
the  assured  advent  of  tabes  constitutes  the  pretabetic 
period.  At  least  twenty  per  cent  of  tabetics  do  not 
know  they  have  syphilis.  Others  have  such  mild  pre- 
tabetic lesions  that  they  are  ignorant  of  the  date  of 
their  infection.  Grossman  !  found  among  240  cases  only 
103  with  a  history  of  a  primary  sore.  The  length  of 
this  pretabetic  interval,  erroneously  styled  the  incuba- 
tion period,  is  therefore  usually  impossible  to  determine 
with  accuracy.  The  duration  of  the  pretabetic  period 
depends  on  the  attacking  force  of  the  spirochete  and  on 
the  weakness  of  the  resistance  of  the  nervous  system. 
The  greater  the  attacking  force  of  the  spirochete  and 
the  weaker  the  defense,  the  shorter  is  the  pretabetic 
interval.  The  duration  of  the  pretabetic  interval  may 
vary  from  a  few  months  to  fifty  years.  Pauly  treated 
a  person  for  a  chancre  on  Sept.  25,  1891,  in  a  public 
hospital  in  Lyons  (Lyon  medicale,  June  12,  1892).  On 
Dec.  21  the  patient  showed  mucous  patches  and  double 
iritis.  On  Jan.  6,  1892,  laryngeal  crises  occurred.  On 
Jan.  25  difficulty  in  standing  was  evident  and  on  Feb. 
8,  about  five  months  after  infection,  ataxia  of  the  legs 
appeared.  Fournier  records  a  case  of  syphilitic  infection 
in  Jan.,  1881,  followed  in  March  of  the  same  year  by 
Romberg's  sign,  lightning  pains  and  diminution  of 
vision. 

Besides    these    fulminating    cases,    tabes    beginning 

1  The  240  cases  of  tabes  analyzed  by  my  assistant,  Dr.  M.  Gross- 
man, comprise  material  from  the  Mt.  Sinai  Hospital  kindly  placed  at 
his  disposal  by  Dr.  B.  Sachs;  material  from  the  Montefiore  Home, 
available  through  the  courtesy  of  Dr.  Wachsman;  and  material  from 
my  service  in  the  Central  and  Neurological  Hospital,  New  York  City. 


DIAGNOSIS  AND  COURSE  OF  TABES       157 

twenty-five  to  thirty  years  after  the  incriminated  infec- 
tion occurs.  Dieulafoy  (Gazette  hebdom.  Aug.  31,  1877) 
reports  a  case  of  syphilis  in  1830,  followed  by  lightning 
pains  in  1865 — in  the  patient 's  sixty-eighth  year — and  by 
diplopia  and  ataxia  in  1870.  Inglerans  (loc.  cit.)  saw  a 
tabetic  who,  in  1861,  at  the  age  of  twenty-six,  acquired 
syphilis  and  who  had  lightning  pains  first  in  1895.  The 
pretabetic  period  in  the  last  two  cases  was  thirty-five 
and  thirty-four  years  respectively.  Among  Grossman's 
240  cases,  the  pretabetic  period  ranged  between  25  and 
32  years  in  thirteen  cases. 

Lewinsky's  70  cases  had  an  average  pretabetic  period 
of  13  years.  In  43  private  cases  in  which  the  infection 
could  be  accurately  dated,  I  found  the  average  preta- 
betic period  was  11.3  years.  Grossman's  240  cases  com- 
prised 136  who  were  ignorant  of,  or  uncertain  about, 
their  infection;  the  103,  who  provided  a  precise  history 
of  chancre,  had  an  average  pretabetic  interval  of  14 
years.  As  there  is  no  agreement  upon  what  constitutes 
the  minimum  essential  for  tabes,  and  as  tabes  may  long 
be  latent  before  the  patient  seeks  the  physician,  even  the 
lowest  of  these  figures,  11.3  years,  is  probably  too  high. 

It  is  affirmed  that  the  shorter  the  pretabetic  period 
the  more  unfavorable  is  the  prognosis.  Von  Malaise 
asserts  that  a  pretabetic  period  of  less  than  six  years 
is  ominous.  Grossman's  series  comprised  13  cases  show- 
ing pretabetic  periods  of  six  years  and  less.  The  average 
pretabetic  period  of  these  13  was  3,9  years ;  none  of  these 
13  has  died ;  their  average  age  is  44  years ;  the  disease 
has  endured  among  them  on  an  average  15.3  years.  A 
short  pretabetic  period  may  be,  but  is  not  necessarily,  an 
unfavorable  sign. 

Erb  states  that  the  younger  a  person  acquires  syphilis, 


158  LOCOMOTOR  ATAXIA 

the  quicker  tabes  follows.  He  reports  a  case  of  infection 
at  191/2  years  followed  by  tabes  at  22.  In  support  of 
this  statement,  Mingazzini  and  Salvador!  record  an  in- 
fection at  18  years  followed  by  shooting  pains  at  19l/o 
years;  and  Schaffer  publishes  a  case  of  infection  at  21, 
leading  to  tabes  at  23.  The  shortest  pretabetic  period 
in  Grossman's  series  was  1^  years  and  occurred  in  a 
man  aged  40^  years.  Grossman  reports  25  cases  of 
tabes  which  referred  their  infection  to  chancres  received 
between  the  ages  of  13  and  20.  The  average  age  of 
infection  of  these  25  was  18.44  years;  among  them 
the  pretabetic  period  varied  from  2  to  Sl1/^  years;  and 
averaged  16.6  years.  Statements  regarding  the  influence 
of  age  on  the  pretabetic  period  should  be  accepted  with 
reserve  until  tables  showing  the  incidence  of  syphilis  and 
tabes  at  all  ages  are  available. 

The  rate  at  which  the  syphilitic  invasion  called  tabes 
spreads  varies  profoundly.  Fournier's  and  Pauly's 
cases  of  rapid  generalization  have  just  been  mentioned. 
Vulpian  records  a  case  in  which  generalization  occurred 
in  four  months;  Rosenthal,  in  five  months;  Trousseau, 
in  six  months;  and  Buzzard,  in  fifteen  months.  I  had 
under  my  care  at  the  Central  and  Neurological  Hospital 
a  case  who  first  sought  advice  for  laryngeal  crises;  he 
had  then  no  knee-jerks,  and  slight  sensory  loss  in  the 
lower  limbs;  next  his  vision  failed  completely  in  one 
eye,  partially  in  the  other;  then  he  developed  general 
paresis.  This  course  occupied  eleven  weeks. 

In  contrast  with  these  rapid  cases  is  a  tabetic  (reported 
by  Raymond)  who  suffered  from  lightning  pains,  dysuria 
and  diplopia  at  the  age  of  forty-one  and  who,  with  no 
knee-jerks  and  fixed  pupils,  still  pursued  his  non-ataxic 
way  at  the  age  of  eighty-six.  Literature  is  crowded  with 


DIAGNOSIS  AND  COURSE  OF  TABES       159 

reports  of  cases  in  which  the  invasion  never  spread. 
Thus,  Dejerine  reports  three  undoubted  tabetics  who 
suffered  for  thirty,  thirty,  and  thirty-six  years  respec- 
tively, only  from  pain :  Fournier,  one  who  for  twenty- 
three  years,  Heldenbergh,  one  who  for  eighteen  years, 
and  Vulpian,  one  who  for  ten  years,  suffered  only  from 
crises.  Raymond  reports  a  tabetic  who  suffered  only 
from  blindness  for  forty-three  years ;  Forster,  one  merely 
blind  for  thirty-three  years.  Schuster  found  seventy- 
eight  abortive  cases  among  five  hundred  tabetics.  Our 
ideas  of  the  spread  of  tabes  have  all  been  clouded  by 
confounding  the  progress  of  the  structural  changes  with 
the  mental  deterioration  which  results  from  them. 

Besides  more  or  less  permanent  arrest  of  the  invasion, 
prolonged  periods  of  quiescence  may  occur.  During 
these  periods  of  quiescence,  the  mental  element  in  symp- 
toms may  spontaneously  lessen.  These  periods  are  hence 
termed  remissions. 

The  interval  between  the  onset  of  tabes  and  the  onset 
of  ataxia  is  called  the  preataxic  period.  We  have  seen 
that  the  onset  of  tabes  cannot  be  absolutely  defined  and 
that  the  onset  of  ataxia,  as  it  usually  is  insidious,  is 
also  difficult  to  date.  The  duration  of  the  preataxic 
period  is  extremely  variable.  Fournier  reported  65 
cases  among  which  the  preataxic  period  lasted  two  years 
or  less  in  19;  more  than  two  years  but  less  than  five  in 
23;  and  from  five  to  fourteen  years  in  23.  In  fifty-four 
per  cent  of  Fournier 's  cases  the  preataxic  period  was 

three  years  or  less. 

In  59  per  cent  of  236  cases  of  Grossman's  series  the 
preataxic  period  was  three  years  or  less. 


160  LOCOMOTOR  ATAXIA 

Grossman's  figures  are  as  folio  war- 
No,  of  cases  Interval  between  the  ascertainable  onset  of 

tabes  and  the  appearance  of  ataxia. 

60  Less  than  6  months 

17  6  months  to  1  year 

24  1  to     2  years 

27  2  to    3     " 

22  3  to    4     " 

20  4  to    5     " 

19  5  to    6     " 

10  6  to    7     " 

12  7  to    8     " 

5  8  to    9     " 

3  9  to  10     " 

4  10  to  11     " 

2  11  to  12  " 
1                                                             13  " 

3  14  to  15  " 
7  15  to  27  " 

The  preataxic  period  is  alleged  to  be  shorter  in  the 
young  and  in  the  old  than  in  the  middle-aged.  If  we 
consider  as  young  those  in  whom  tabes  begins  at  or 
before  the  age  of  30;  and  as  old,  those  in  whom  tabes 
begins  at  or  after  the  age  of  50,  Grossman's  series  shows 
35  young  of  whom  11  had  a  preataxic  period  of  1  year 
or  less ;  33  old  of  whom  16  were  preataxic  for  1  year  or 
less,  and  170  between  the  ages  of  30  and  50,  of  whom  57 
were  preataxic  for  1  year  or  less.  The  preataxic  period 
was  1  year  or  less  in  31  per  cent  of  the  young ;  in  48  per 
cent  of  the  old,  and  in  31  per  cent  of  the  remainder. 

The  preataxic  period  is  prolonged  in  the  blind.  Cases, 
at  my  disposal,  of  ataxia  following  blindness  are  too  few 
to  permit  any  estimation  of  the  duration  of  the  preataxic 
period  in  the  blind.  Statistics  of  the  duration  of  the 


preataxic  period  have  little  absolute  value.  Fournier 
has  published  a  further  list  of  86  cases  in  which  ataxia 
had  not  yet  appeared.  The  duration  of  these  cases 
ranged  from  1  to  30  years;  the  average  duration  was 
5.7  years.  Cases  of  forty  and  of  fifty-five  years'  duration 
without  ataxia  have  been  recorded. 

The  ataxic  stage  dates  from  the  onset  of  ataxia  to  the 
onset  of  helplessness.  It  is  said  to  last  from  ten  to 
twenty  years.  Most  tabetics  perpetuate  the  ataxic  stage 
and  never  become  bedridden. 

Grossman's  series  comprises  36  so-called  "paralytic" 
cases — chair-  or  bedridden  tabetics. 

Six  cases  had  been  immobile  for  one  year  or  less ;  six 
for  more  than  one  but  less  than  three  years ;  twelve  for 
three  to  four  years;  four  for  more  than  four  but  less 
than  eight  years ;  four  for  eight  to  twelve  years.  Twenty 
of  these  cases  had  been  immobile  from  three  to  twelve 
years.  The  duration  of  the  immobile  period  is  deter- 
mined mainly  by  the  nurse. 

The  remaining  four  of  these  immobilized  patients  died ; 
one  at  the  age  of  30,  after  four  years  of  bed  existence, 
from  pylonephrosis  and  pneumonia;  another  aged  39, 
after  three  months  in  bed,  from  pylonephrosis;  a  third, 
50  years  old,  bedridden  for  12  years,  from  arterio- 
sclerosis ;  a  fourth,  aged  49,  after  seven  months  immobil- 
ity, from  an  unascertained  cause. 

Among  these  immobile  tabetics  there  are  three  main 
groups;  one,  containing  16  cases  immobilized  by  ataxia 
complicated  by  other  factors,  such  as  joint  trouble  and 
fractures;  another,  containing  five  non-ataxic  cases  im- 
mobilized by  blindness -or  injuries,  and  a  third  containing 
15  cases  immobilized  by  ataxia  alone. 

Among  the  16  ataxies  forming  the  first  group,  immo- 


162  LOCOMOTOR  ATAXIA 

bilization  followed  in  5  cases  the  concurrence  of  blind- 
ness and  ataxia,  and  in  5  others,  the  appearance  of 
Charcot  joints;  2  cases  were  attributed  to  fracture 
and  Charcot  joints;  1  to  fracture  without  joint  trouble; 
one  to  intraspinal  medication;  one  to  perforating  ulcer 
in  the  foot,  and  one  to  muscular  atrophy,  complicating 
ataxia.  The  tabetic  who  blamed  intraspinal  medication 
for  his  bedridden  state  was  aged  72.  After  5  years 
contending  with  gastric  crises,  he  became  ataxic.  He 
persisted  active  for  7  years  more.  Intraspinal  medica- 
tion was  his  last  hope  and  when  it  failed  he  gave  up 
the  struggle.  Only  in  a  single  case,  which  was  bedridden 
because  of  muscular  atrophy,  could  a  real  paralytic  stage 
be  distinguished.  Of  5  in  the  second  group  none  have 
had  ataxia:  three  took  to  bed  and  remained  there  after 
injury  to  their  lower  limbs;  2  after  the  onset  of  blind- 
ness. Of  the  15  immobilized  because  of  ataxia  alone, 
2  retired  to  bed  immediately  ataxia  appeared.  Among 
the  6  who  became  bedridden  within  4  years — six,  six, 
twelve,  eighteen,  twenty-four  and  fourty-two  months 
after  the  appearance  of  uncomplicated  ataxia — the  pre- 
ataxic  period  was  2  years  or  less  in  5. 

The  insatiable  instinct  "to  distinguish'*  which  the 
physician  shares  with — perhaps,  inherits  from — the 
scholastic,  has  led  to  the  differentiation  of  myriads  of 
types  of  tabes.  We  distinguish  pain  types,  crises  types, 
bladder  types,  ataxic  types,  blind  types  and  deaf  types, 
sensory  types  and  motor  types,  tardy  types  and  ful- 
minating types,  juvenile  tabes,  adolescent  tabes,  senile 
tabes,  spinal,  sacral,  lumbar  and  dorsal  tabes,  cervical, 
bulbar  and  optic  tabes;  and  so  forth  endlessly. 

From  the  unreliable  point  of  the  appearance  of  the 
first  symptom,  the  age  at  the  onset  of  tabes  is  calculated. 


DIAGNOSIS  AND  COURSE  OF  TABES       163 

It  has  no  limits;  tabes  may  appear  in  childhood  and  in 
adolescence  as  well  as  in  middle  age.  I  have  seen  two 
in  whom  tabes  first  appeared  after  their  fifty-fifth  year. 
Several  over  70  years  old  have  been  recorded. 

Moebius,  Karger,  Berger  and  Friedrichsen  record  a 
total  of  seventy-four  tabetic  women  among  whom  tabes 
occurred  in  sixty-six  (89  per  cent)  before  the  age  of 
fifty ;  and  in  all  before  sixty.  Under  twenty-five  years  of 
age,  seven  cases  occurred ;  after  fifty,  eight ;  and  between 
twenty-five  and  fifty,  fifty-nine.  Of  one  hundred  and 
eighty-five  cases  recorded  by  Erb  and  Karger,  two  per 
cent  occurred  before  twenty  years  of  age;  ten  per  cent 
before  thirty ;  sixty  per  cent  before  forty ;  and  ninety  per 
cent  before  fifty.  Tabes,  therefore,  occurs  usually  be- 
tween the  ages  of  thirty  and  forty-five ;  and  is  rare  after 
fifty  and  before  twenty-five.  The  age  incidence  of  tabes 
in  Grossman's  series  has  already  been  mentioned. 

To  estimate  the  average  age  of  onset  of  tabes  we  must 
ignore  the  rare  cases,  the  cases  after  fifty  and  before 
twenty-five.  Of  the  Moebius  series  the  average1  age  at 
onset  was  thirty-five  and  a  half  years;  of  Erb  and  Kar- 
ger's  series  thirty-eight  years;  of  seventy-eight  cases 
which  I  saw  within  seven  years  of  the  onset  of  the  dis- 
ease, 36.9  years;  of  239  cases  collected  by  Grossman 
39.1  years. 

The  average  age  at  death  in  33  out  of  the  34  cases 
reported  by  Burr  was,  53.46  years;  in  19  cases,  57  per 
cent,  death  occurred  at  53  years  or  later.  The  average 
age  at  death  of  the  28  cases  in  Grossman's  series,  was 
also  53  years:  in  15  cases,  53  per  cent,  death  occurred 
at  53  years  or  later.  In  Grossman's  series  there  were  77 

1  All  averages  are  arithmetical  means,  except  those  of  my  cases  which 
are  probable  means  (Wahrscheinliche  Mittel). 


164  LOCOMOTOR  ATAXIA 

tabetics  aged  53  years  or  more.  The  death  rate  among 
tabetics  of  53  years  or  more  was  therefore  195  per  thou- 
sand. 

The  causes  of  death  in  tabes  are  two — cardiovasculo- 
renal  disease,  and  adventitious  infections,  such  as  cysti- 
tis, pyonephrosis,  pneumonia  and  tuberculosis.  The  spi- 
rochete  attacking  the  central  nervous  system  produces 
simultaneously  less  obvious  but  sometimes  more  grave 
lesions  in  the  cardiovascular  system;  and  such  lesions 
may  be  aggravated  by  the  massive  doses  of  the  metallic 
poisons,  mercury  and  arsenic,  which  are  used  to  combat 
the  spirochete.  The  concurrence  of  syphilis  and  tubercle 
is  always  menacing;  there  exists  no  proof  that  tuber- 
culosis is  more  lethal  to  the  tabetic  than  to  any  other 
syphilitic.  The  liability  of  the  tabetic  to  tuberculosis 
has  not  been  proved  to  be  greater  than  that  of  the  non- 
tabetic  syphilitic.  But  an  imperfect  resistance  which 
renders  the  central  nervous  system  liable  to  attack  may 
make  tabetics  prone  to  intercurrent  affections  and  the 
resistance  may  be  still  further  reduced  by  the  vegetative 
lesions  of  tabes. 

None  ever  dies  of  tabes,  just  as  none  ever  dies  of 
blindness,  or  of  deafness,  or  of  other  sensory  defect. 

The  lethality  of  tabes  is  that  of  syphilis.  Raymond's 
tabetic,  hale  and  hearty  at  the  age  of  eighty-six;  and 
Trousseau's  octogenarian  tabetic,  possessed  of  a  "vig- 
ueur  insolite  a  son  age ' '  show  how  "benign  tabes  may  be. 


CHAPTEE  IX 

ANTISYPHILITIC  TREATMENT  IN  TABES 

Essential  tabetic  lesion  irreparable.  Tabes  incurable.  Effect  of  an- 
tisyphilitic  treatment  on  the  duration  of  the  pretabetic  period. 
Absence  of  proof  that  such  treatment  can  prevent  tabes.  Nature 
of  the  evidence  required  to  establish  such  preventive  action.  Ab- 
sence of  proof  that  antisyphilitic  substances  arrest  tabes.  Nature 
of  the  evidence  required  to  establish  the  power  of  a  drug  to  ar- 
rest tabes.  Drugs  commonly  used  in  tabes.  Mercury :  modes  of 
administration.  Arsenic,  enesol,  salvarsan.  Motives  for  intra- 
spinal  administration  unfounded.  The  search  for  new  prepara- 
tions of  antisyphilitic  substances  and  for  new  methods  of  ad- 
ministration :  indications  of  the  inadequacy  of  these  substances. 
Necessity  for  caution  in  the  use  of  *mercury  and  arsenic  in  tabes. 
Nucleinates  and  nucleinic  acid. 

THE  fundamental  lesion  of  tabes  is  a  degeneration  of 
the  nerve  processes.  Whether  this  degeneration  occurs 
in  the  spinal  roots,  or  in  the  optic  nerve,  or  elsewhere,  it 
is  not  secondary  to  meningeal  inflammation  but  is  a  result 
of  invasion  of  the  nerve  processes  themselves.  Any 
meningeal  inflammation  which  occurs  is  a  concomitant, 
a  more  or  less  accidental  complication  of  the  invasion 
of  the  nerve  processes  (p.  20). 

Tabetic  degeneration  occurs  essentially  in  nerve  proc- 
esses which  lack  the  protection  of  the  neurilemmal 
sheath,  the  sheath  of  Schwann.  It  may  be  laid  down  as 
an  axiom  that  nerves  in  which  Schwann 's  sheath  is  ab- 
sent, nerves  such  as  constitute  the  white  matter  of  the 
central  nervous  system,  when  once  degenerated,  do  not 
spontaneously  regenerate.  Any  medication  which  cannot 
be  demonstrated  to  have  the  power  to  regenerate  nerves, 

165 


166  LOCOMOTOR  ATAXIA 

cannot  cure  a  disease  in  which  degeneration  of  nerves 
occurs.  A  considerable  remedial  influence  can  be  exerted 
upon  the  inflammatory  exudates  which  accompany  syph- 
ilitic invasion  of  nerve  processes  and  upon  the  prolifera- 
tion in  the  meninges — when  such  exists — by  means  of 
iodids,  mercury,  arsenic  and  other  antisyphilitic  reme- 
dies. As  objective  evidence  of  this  influence,  we  find  a 
change  in  the  nature  of  the  Wassermann  reaction,  and 
a  decrease  of  the  cellular  elements  in  the  cerebrospinal 
fluid;  exceptionally,  a  less  sluggish  tendon  reflex,  a  less 
fixed  pupil:  as  subjective,  a  diminution  in  some  symp- 
toms, particularly  pain.  Apart  from  the  removal  by 
medicinal  means  of  exudates  and  of  the  syphilitic  tissue 
overgrowth,  which  in  the  meninges  may  impair  function, 
or  even  cause  destruction  of  the  reflex  paths,  it  is  certain 
that  we  can  by  no  measures  now  at  our  disposal  repair 
the  affected  structures  in  tabes.  As  we  know  no  sub- 
stance which  will  cure  the  nerve  degeneration  which  is 
the  essential  lesion  of  tabes,  we  know  no  cure  for  tabes. 
Inquiry  elicits  that  some  tabetics  receive  no  anti- 
syphilitic  treatment  for  their  pretaToetic  lesions;  that 
others  receive  merely  cursory  treatment ;  and  that  others 
again  receive  what  even  the  captious  must  consider 
adequate.  No  proof  was  ever  offered  that  the  non-tabetic 
receive  more  antisyphilitic  treatment  than  the  tabetic. 
Many  pretabetics  receive  cursory  treatment  because  of 
the  trivial  nature  of  their  syphilids.  These  trivial 
syphilids  are  evidence  of  a  trivial  reaction  to  the  spiro- 
chete  and  of  a  trivial  production  of  defense  substances. 
This  trivial  reaction  may  be  adequate  to  kill  the  spiro- 
chete :  some  syphilitics  have  but  mild  syphilids  and  have 
no  subsequent  symptoms.  But  others  owe  to  the  mildness 
of  the  pretabetic  lesions  the  inadequacy  of  the  defensive 


ANTISYPHILITIC  TABES  TREATMENT     167 

substances  produced  by  the  outpost  tissues,  which  leads 
to  the  persistence  of  the  spirochete  and  later  to  the 
development  of  tabes. 

Noehte  states  that  pretabetic  antisyphilitic  treatment 
has  no  influence  upon  the  later  appearance  and  course 
of  tabes.  Lewinsky  reports  that  the  average  interval 
between  the  primary  syphilitic  infection  and  the  first 
symptom  of  tabes  in  a  series  of  tabetics  which  he  inves- 
tigated was  as  follows : — 

A.  In  untreated  cases  (14  men,  1  woman),  fourteen 
years. 

B.  In  cases  inadequately  (unzulanglich)  treated  (39 
men,  10  women),  thirteen  years. 

C.  In  cases  fully   (ausreichlich)   treated   (5  men,   1 
woman),  eleven  years. 

Lowinsky  unexpectedly  makes  these  statistics  a  basis 
for  a  plea,  not  against,  but  on  behalf  of,  energetic  anti- 
syphilitic  treatment  in  the  pretabetic.  Lewinsky's  fig- 
ures must  not  be  unduly  emphasized.  I  have  found  no 
difference  in  the  age  of  onset  of  tabes  among  those  who 
were  cognizant  and  those  who  were  ignorant  of  their 
syphilitic  infection;  among  those,  in  other  words,  who 
presumably  were  treated  and  those  who  were  not. 

As  tabes  does  not  necessarily  follow  untreated  or  cur- 
sorily treated  syphilis;  as  tabes  may  occur  in  spite  of 
intensive  antisyphilitic  treatment;  and  as  antisyphilitic 
treatment  may  not  lengthen,  and  may  even  be  associated 
with  a  shortening  of,  the  pretabetic  period,  the  value  of 
antisyphilitic  treatment  in  preventing  tabes  needs  proof. 

To  ascertain  if  we  can  prevent  tabes  by  treatment,  we 
must  know  how  often  tabes  occurs  in  untreated  and  in 
treated  syphilis,  respectively.  The  civilized  are  subject 
to  and  the  primitive  are  free  from  antisyphilitic  treat- 


168  LOCOMOTOR  ATAXIA 

ment  and  tabes.  Too  many  other  differences  distinguish 
civilized  from  primitive  races  to  permit  any  conclusions 
regarding  the  causal  relation  of  antisyphilitic  treatment 
to  tabes  to  be  drawn  from  this  fact.  In  the  same 
race  the  ratio  of  tabes  to  syphilis  varies  according  to 
sex,  environmental,  occupational  and  constitutional  con- 
ditions. To  ascertain  the  effect  of  treatment  in  pre- 
venting tabes  we  must  eliminate  as  many  as  possible  of 
these  apparent  sources  of  variation.  If  investigation 
be  narrowed  to  males  of  the  same  race,  age,  social  condi- 
tion and  occupation,  the  larger  the  number  considered, 
the  more  will  any  other  sources  of  error,  such  as  differ- 
ences in  individual  resistance  and  in  the  virulence  of  the 
infecting  spirochete,  be  discounted.  The  ideal  field  for 
such  an  investigation  is  the  services.  There,  competent 
observers  have  care  of  large  bodies  of  men  who  are 
approximately  of  the  same  age,  civilization  and  social 
standing ;  who  are  similarly  employed ;  who,  if  syphilitic, 
are  skillfully,  equally  and  assiduously  treated;  and  who 
can  be  observed  for  years.  The  frequency  of  syphilis 
among  these  men  should  be  ascertained  by  blood  •exami- 
nation. Vedder  has  already  made  a  notable  beginning  by 
examining  the  United  States  recruits.  If  from  the  ser- 
vices we  can  only  ascertain  the  frequency  with  which 
syphilitic  disease  of  the  nervous  system  occurs  in  treated 
syphilis,  we  shall  be  able  to  compare  with  that  the  fre- 
quency in  analogous  groups  of  less  treated  civilians. 
Even  from  this  evidently  inaccurate  comparison  we  shall 
gain  some  knowledge  of  the  power  or  impotence  of  ac- 
cepted antisyphilitic  remedies  to  prevent  invasion  of  the 
nervous  system.  At  present  we  have  no  knowledge :  only 
unverified  tradition  and  belief. 

To  prove  that  a  drug  can  arrest  tabes,  we  must  know 


the  rate  at  which  tabes  advances.  Few  things  are,  how- 
ever, so  variable  as  this  rate.  Tabes  may  advance  with 
fulminating  rapidity;  may  progress  insidiously  and  this 
progress  may  be  punctuated  by  sudden  exacerbations 
and  remissions ;  or  may  commence,  advance  slightly,  and 
then  spontaneously  stop.  Schuster  found  seventy-eight 
abortive  cases  among  five  hundred  tabetics. 

Therefore,  in  a  given  case,  we  cannot  foretell  the  rate 
of  progress  in  tabes,  nor  may  we  affirm  the  causal  rela- 
tion between  the  administration  of  a  drug  and  the  arrest 
of  the  tabetizing  process.  If  we  could  observe  a  suffi- 
ciently large  series  of  cases  of  tabes  for  a  period  wherein 
definite  advance  in  the  lesions  of  tabes  might  be  ex- 
pected, and  if  of  this  series  half  of  the  cases  were 
reserved  as  a  standard,  and  were  given  no  medication, 
wliile  the  other  half  were  treated  with  the  alleged  remedy, 
we  could  reach  conclusions  which,  although  not  permit- 
ting unrestricted  generalization,  yet  would  be  of  notable, 
value.  In  the  absence  of  such  data,  a  physician  who 
states  that  a  drug  has  arrested  tabes  relies  on  a  prog- 
nostic acumen  which  is  denied  to  his  fellows:  his  state- 
ment exposes  him  not  only  to  credit  for  supposed  suc- 
cess but  also  to  blame  for  failure. 

A  substance  averred  to  arrest  tabes  must  be  able  to 
stop  the  advance  of  tabes.  It  is  upon  the  failures  to 
stop  advance,  not  upon  alleged  arrests,  that  judgment 
of  remedies  in  a  disease  of  such  uncertain  course  as  tabes 
should  be  based.  Every  neurologist  observes  the  fail- 
ure of  antisyphilitic  remedies  to  prevent  the  advance  of 
tabes  with  a  frequency  which  is  greater  the  larger  his 
practice  in  tabes.  Dejerine  could  detect  no  influence  of 
mercury,  and  I  no  influence  of  salvarsan,  on  tabetic  optic 
atrophy. 


170  LOCOMOTOR  ATAXIA 

Professor  Warthin  by  a  long  and  careful  study  was 
able  conclusively  to  demonstrate  post  mortem  in  a  series 
of  cases  of  tabes  and  other  forms  of  old  syphilis  the  pres- 
ence of  the  spirochete  in  the  tissues,  not  merely  of  those 
who  had  received  intensive  antisyphilitic  treatment,  but 
even  in  those  who  because  of  that  treatment  "had  attained 
before  death  a  negative  Wassermann  reaction. 

We  know  no  drug  which  can  cure  tabes,  and  we  are 
uncertain  of  the  power  of  antisyphilitic  remedies  to  pre- 
vent or  to  arrest  tabes.  Our  reaction  to  this  ignorance 
is  reflected  in  the  drug  treatment  of  tabes.  The  more 
unsatisfactory  the  medicinal  treatment  of  a  disease 
proves,  the  more  numerous  are  the  drugs  lauded  as  effi- 
cacious. When  we  possess  a  specific  for  a  disease,  as 
quinine  for  malaria,  it  reigns  alone.  There  are  few 
drugs  in  the  pharmacopoeia  which  have  not  been  invoked 
to  aid  the  tabetic.  Those  which  have  been  most  used 
are  silver,  mercurial  and  arsenical  preparations,  and 
the  alkaline  iodids.  Silver  salts  were  fashionable  until 
the  frequency  of  argyria  made  them  lose  favor.  Iodids 
were  employed  to  aid  the  absorption  of  the  inflammatory 
products  of  syphilis,  but,  as  they  were  not  dramatic  in 
action  and  as  they  habitually  were  given  in  doses  so 
small  that  little  reached  the  cerebrospinal  system,  and 
all  was  speedily  excreted,  they  fell  into  unmerited  dis- 
use. 

With  the  growing  belief  that  syphilis  caused  tabes,  all 
except  antisyphilitic  substances  ceased  to  be  employed. 
Mercury  was  long  the  chosen  drug.  It  formerly  was 
given  by  the  mouth.  Inaccuracy  of  dosing  and  other 
disadvantages  led  to  oral  administration  being  replaced 
by  inunction.  Inunction  combined  quick  absorption  of 


ANTISYPHILITIC  TABES  TREATMENT     171 

the  mercury  not  only  with  the  useful  measures  of  mas- 
sage and  bathing,  but  also  with  the  psychic  influence  of 
the  rubber.  These  rubbers,  especially  at  Aix-la-Chapelle, 
where  they  constitute  a  class  with  almost  hereditary 
privileges,  were  skilled  to  exert  a  beneficent  mental  ef- 
fect upon  the  tabetic,  the  most  suggestible  of  all  patients. 
Added  to  the  mercury,  bathing,  massage,  and  rubber, 
was  the  psychotherapeutic  influence  of  the  spa.  The  dis- 
tracted tabetic  removed  from  his  usual  environment,  was 
disciplined ;  his  regime  was  regulated ;  the  spa  physician 
was  a  health-giver  whose  dictum  was  law;  and  the  tabetic, 
in  salutary  competition  for  health,  strove  with  the  simi- 
larly sick.  No  device  was  missing  to  reinforce  the  psy- 
chic effect  of  mercurial  inunction:  so  inunctions  con- 
ferred, and  still  confer,  benefit. 

Inhalation  was  offered  unsuccessfully  as  a  rival  to 
inunction,  which,  however,  was  later  somewhat  displaced 
by  injection.  As  injections  proved  too  irritating  when 
subcutaneous,  they  were  made  intramuscular.  Then,  to 
avoid  soaking  all  tissues  in  mercury,  in  order  to  induce 
with  the  surplus  an  influence  upon  the  central  nervous 
system,  intraspinal  injection  was  introduced.  At  first 
careless  experimenters,  forgetting  the  irritation  that 
followed  even  subcutaneous  injection,  used  salts,  such 
as  the  perchlorid,  which  precipitate  the  albumen  of  any 
tissue  they  encounter  and  act  as  destructive  agents  at  the 
site  of  the  injection.  Success  did  not  follow,  and  the 
next  step,  direct  administration  to  the  diseased  part,  was 
made  by  Horsley.  I  occasionally  assisted  him  when  he 
trephined  for  gummata  and  laved  the  meningeal  surface 
with  perchloride  of  mercury. 

During  the  greatest  vogue  of  mercury,  arsenic  in  one  or 
other  of  its  pharmacopoeial  preparations  was  also  used, 


172  LOCOMOTOR  ATAXIA 

sometimes  alone,  sometimes  in  combination  with  iodids, 
or  with  mercury.  Then  proprietary  compositions,  such 
as  enesol,  were  in  turn  devised,  lauded  and  forgotten. 
Such  was  our  consciousness  of  the  failure  of  these  sub- 
stances that  Ehrlich's  announcement  of  salvarsan  was 
welcomed  almost  universally.  The  enthusiasm  of  the 
protagonists  of  salvarsan  inadvertently  created  a  cult 
which  was  ludicrously  like  that  created  by  the  two 
thieves  in  Grimm's  fairy  tale  who  sold  silk  which  re- 
mained invisible  to  all  who  were  unworthy  to  exercise 
the  function  of  the  position  which  fate  had  bestowed 
upon  them.  Salvarsan  began  its  clinical  career  as  an 
injection,  usually  intravenous.  Its  lethality  to  the  spiro- 
chete  was  said  to  be  so  much  greater  than  its  toxicity  to 
human  cells  that  by  its  aid  the  destruction  of  every 
spirochete  in  every  nook  of  the  body  was,  at  first,  con- 
sidered feasible.  The  extravagance  of  these  initial 
hopes  soon  remained  only  with  the  laity.  Powerful  and 
speedy  as  was  the  action  of  salvarsan  upon  pretabetic 
lesions,  it  proved  perhaps  even  less  permanent  than  the 
action  of  mercury.  McDonagh  suggested  that  the  spiro- 
chete has  an  inactive,  resistant,  spore-forming  stage  in 
which  it  is  impervious  to  salvarsan. 

The  failure  of  salvarsan  in  syphilitic  nervous  lesions 
was  admitted  by  Ehrlich  when  he  stated  that  salvarsan 
was  an  adjuvant  to  the  human  defensive  substances,  and 
that  defensive  substances  were  present  in  the  blood  but 
absent  from  the  cerebrospinal  fluid. 

Meanwhile,  Willcox  claimed  that  after  intravenous  ad- 
ministration of  salvarsan,  arsenic  occurred  in  no  con- 
siderable quantity  in  the  brain,  although  plentifully  pres- 
ent in  other  organs,  such  as  the  liver  and  kidneys ;  and 
Camp,  that  it  was  missing  from  the  cerebrospinal  fluid. 


So  therapeutists  injected  salvarsan  intravenously;  after 
forty-five  minutes,  withdrew  blood  from  the  injected  per- 
son; and  then  introduced  the  salvarsanized  serum  intra- 
spinally.  Thus  they  ingeniously  placed  a  minute  dose 
— about  0.2  milligrams — of  a  benign  form  of  salvarsan, 
plus  the  necessary  defensive  substances,  in  contact  with 
the  diseased  tissues  in  the  cord.  Benedict  now  proves 
that  the  intravenous  produces  a  greater  concentration  of 
salvarsan  in  the  cerebrospinal  fluid  than  does  such  intra- 
spinal  administration.  He  injected  salvarsan  intraven- 
ously and  fifteen  to  forty-five  minutes  later,  estimated  its 
amount  in  the  blood.  After  twenty-four  hours  he  found 
salvarsan  not  only  present  in  the  cerebrospinal  fluid  but 
present  still  in  one-sixth  to  one-tenth  the  concentration 
he  first  found  in  the  blood. 

Yet  many  never  permit  themselves  to  realize  that  these 
drugs  frankly  fail  in  tabes;  only  the  method  of  using 
them  may  be  acknowledged  faulty;  hence,  new  methods 
of  administration  are  invented  and  the  life  of  the  false 
specific  is  artificially  prolonged  by  fresh  groups  of  the 
credulous.  Thus,  there  is  now  appearing  in  lay  and  in 
medical  journals  an  attempt  to  replace  needless  intra- 
spinal,  by  intracerebral,  or  by  intraventricular  injection 
of  salvarsan  and  of  mercury.  Those  who  calmly  advise 
such  treatment  ignore  the  mortality  inseparable  from 
trephining;  ignore  the  prodigious  shock  of  the  opera- 
tion to  those  who  survive;  ignore  the  fact  that  direct 
application  of  the  drug  to  the  spinal  cord  failed  to  arrest 
the  syphilitic  lesions  there;  and  in  their  reports  some- 
times show  ignorance  even  of  the  principles  which  should 
govern  their  investigation,  if  their  dangerous  procedure 
be  meant  to  have  any  experimental  value. 

The  lack  of  success  of  antisyphilitic  substances  is  ac- 


174  LOCOMOTOR  ATAXIA 

knowledged  in  the  incessant  changes  which  are  made  in 
the  form  and  in  the  method  of  their  administration.  Yet 
all  are  agreed  that  their  failure  is  not  absolute.  We 
sometimes  achieve  slight,  if  temporary,  success  in  the 
relief  of  tabetic  symptoms  by  these  substances.  The 
aid  is  not  wholly  due  to  the  drug:  the  physical  effects 
of  massage  and  baths  in  mercurial  inunction  and  of 
lumbar  puncture  in  intraspinal  injections ;  and  the  mental 
influence  inseparable  from  all  medicinal  treatment,  must 
be  credited  with  some  share  in  any  improvement  which 
results.  The  rest  of  their  aid  is  mainly  due  to  the  so- 
called  alterative  effect,  the  effect  upon  the  vegetative 
nervous  system,  which  arsenic,  mercury  and  iodids  pro- 
duce ;  and  to  the  solvent  action  of  these  drugs  upon  men- 
ingeal  and  interstitial  exudates,  the  accidental  and  non- 
essential  accompaniments  of  the  syphilitic  invasion  of 
nerve  processes. 

In  default  of  more  certain  remedies,  we  must  still 
avail  ourselves  of  any  aid  which  these  substances  lend. 
But  the  limitations  of  such  aid  should  be  clearly  recog- 
nized. We  should  realize  that  mercury  and  salvarsan, 
so  valuable  in  removing  banal  syphilitic  lesions,  have  not 
been  proved  to  have  demonstrable  value  in  syphilitic  le- 
sions of  the  essential  cells  of  usually  sheltered  tissues. 
Renal,  hepatic,  cardiac,  vascular,  and  nervous  parenchy- 
matous  lesions  of  syphilitic  origin  are  all  resistant  to 
antisyphilitic  remedies.  Their  obstinacy  to  treatment  is 
due  in  part  to  the  restricted  capacity  of  the  essential 
cells  of  these  highly  specialized  tissues  to  repair  and  to 
regenerate.  Mercury  and  arsenic  are  powerful  proto- 
plasmic poisons.  They  are  generally  considered  to  be 
contraindicated  in  non-syphilitic  cardiac  and  renal  dis- 
eases. Cardiac  and  renal  diseases  not  infrequently  bring 


ANTISYPHILITIC  TABES  TREATMENT     175 

death  to  the  tabetic.  The  nebulous  aid  of  these  sub- 
stances in  tabes  should,  therefore,  be  sought  as  cau- 
tiously as  it  is  now  sought  recklessly. 

Nucleinic  acid  and  nucleinate  of  soda  have  been  much 
lauded,  especially  in  paresis.  They  produce  a  leucocy- 
tosis  which  is  mainly  mononuclear.  After  each  injec- 
tion, a  transient  febrile  reaction  occurs.  Gradually  an 
immunity  to  the  drug  develops,  so  that  greater  and 
greater  doses  are  necessary  to  induce  any  reaction.  The 
aim  in  treatment  is  to  prolong  the  reactive  period  as 
much  as  possible;  hence,  small  doses  are  used  at  first, 
and  an  increase  is  made  only  when  the  temperature  and 
the  blood  count  show  that  the  dose  last  used  is  no  longer 
capable  of  producing  a  characteristic  effect.  Strict 
aseptic  precautions  are  necessary  to  prevent  the  occur- 
rence of  inflammation  at  the  site  of  injection.  I  have 
used  the  nucleins  both  with  and  without  the  massive 
doses  of  salvarsan  now  advocated.  In  fourteen  cases  in 
which  the  nucleinate  of  soda  was  used,  for  several 
months,  in  which  immunity  to  doses  as  high  as  two 
grams  was  achieved,  I  heard  great  reports  from  pa- 
tients, but  saw  neither  objective  nor  persistent  subjec- 
tive improvement  in  tabes.  Indeed,  one  of  my  tabetics 
developed  paresis  after  a  three  months'  course  of  nuclei- 
nates,  and  quickly  died. 


CHAPTER  X 

THE  MENTAL  STATE  OF  TABES 

Mental  stress  a  cause  of  tabes.  Tabes  a  source  of  mental  stress.  Tabes 
a  cause  of  fear,  of  fatigue,  and  of  depression.  Psychoses  in  tabes. 
The  psychosis  typical  of  tabes  an  aggravation  of  the  mental  state 
induced  by  the  tabetic  symptoms.  Resemblance  between  tabetic 
psychoses  and  prison  psychoses.  Measurement  of  the  mental  state 
of  the  tabetic.  Weakening  of  attention  in  tabes:  its  sensory  and 
motor  effects.  Variations  in  the  mental  state  of  tabes.  Mental 
deterioration:  its  rate  and  its  consequences.  Influence  of  the 
tabetic  symptoms  upon  the  mental  state.  Influence  of  the  mental 
state  upon  the  tabetic  symptoms.  Estimation  of  the  reciprocal 
relations  of  the  tabetic  symptoms  and  the  mental  state.  Interde- 
pendence of  tabetic  symptoms.  Foundations  of  mental  treatment. 

THE  ratio  of  tabes  to  syphilis  is  higher  in  civilized  than 
in  primitive  peoples,  in  men  than  in  women,  in  the  intel- 
lectual than  in  the  working  classes.  A  factor  in  deter- 
mining this  incidence  is  mental  stress. 

Life  with  tabes  is  exhausting.  To  endure  pain,  crises, 
and  other  manifestations  of  tabes  taxes  the  strongest; 
to  work  in  pain  and  fear  and  depression  requires  strenu- 
ous effort;  to  move  with  incoordinate  limbs  is  a  hercu- 
lean task.  The  effort  demanded  by  day  soon  exceeds  the 
recuperation  gained  in  the  painful,  sleepless  nights. 
Slighter  and  slighter  efforts,  either  mental  or  physical, 
fatigue  the  tabetic,  quicken  his  pulse  and  respiration, 
cause  palpitation  and  breathlessness. 

The  many  perils  to  which  the  ataxic  is  exposed  become 
increasingly  harassing.  His  incapacity  fills  him  with 
anxiety  regarding  his  business  and  the  sustenance  of  his 
family.  To  these  worries,  he  adds,  in  many  cases,  fear 

176 


THE  MENTAL  STATE  OF  TABES  177 

lest  his  wife  or  his  child  acquire  the  disease.  He  dreams 
of  failure,  of  fires,  of  drowning,  of  starving  on  a  raft 
in  the  midst  of  a  limitless  sea,  of  all  kinds  of  catastro- 
phes. Fear  complexes,  as  they  elaborate,  more  and 
more  immediately  succeed  one  another,  until  they  pro- 
duce an  unrelieved  state  of  perturbation.  A  veritable 
anxiety  neurosis  develops  and  extravagant  manifesta- 
tions of  fear  arise  from  the  most  trivial  occurrences. 
Thus,  the  tabetic  may  show  dread  of  the  dark,  of  the 
open,  of  change  of  level,  of  change  of  surface,  of  cross- 
ings, of  traffic,  of  strange  places,  of  unaccustomed  furni- 
ture, of  company  other  than  that  of  his  family. 

As  the  tabetic  is  attacked  by  one  after  the  other  of 
the  unexpected,  bewildering  and  mysterious  manifesta- 
tions of  tabes,  he  loses  heart.  Unenlightened  treatment 
fails  to  relieve  him.  The  disease  obviously  and  relent- 
lessly advances.  He  feels  increasingly  his  lack  of  com- 
petence to  cope  with  his  business,  social  and  domestic 
affairs,  and  he  becomes  more  and  more  depressed.  This 
depression  deepens  till  trivial  impersonal  occurrences, 
such  as  a  gray  day,  produce  altogether  disproportionate 
results.  Depression  occasionally  leads  to  drink,  suicide, 
or  an  insane  asylum. 

The  tabetic,  fearful,  irritable,  depressed,  weary,  sleep- 
less and  emaciated,  becomes  less  and  less  competent.  He 
increasingly  distrusts  his  sensations.  He  is,  therefore, 
more  and  more  shut  off  from  his  environment.  Deaf- 
ness and  failing  vision  may  add  to  his  misery. 

Everyone  has  a  definite  degree  of  ability  to  withstand 
mental  strain.  The  degree  varies;  some  are  so  consti- 
tuted that  they  cannot  long  tolerate  even  the  average 
stress  of  modern  life.  The  limit  of  endurance  may  be 
passed  suddenly  as  the  result  of  a  shock,  or  gradually, 


178  LOCOMOTOR  ATAXTA 

in  consequence  of  prolonged  fatigue.  Beyond  the  limit 
of  endurance  psychoses  develop.  The  psychoses  of  tabes 
have  been  recorded  by  Meyer,  Rydlewski,  Henderson  and 
others.  They  report  cases  of  mental  disease  acci- 
dentally occurring  in  tabes,  together  with  cases  which 
are  due  to  tabes. 

Of  fifty-four  psychoses  encountered  in  tabetics  by 
Meyer,  twenty-one  were  chronic  hallucinatory  parano- 
ias ;  fourteen,  depressive  psychoses ;  six,  dementias ;  five, 
hallucinatory  conditions;  four,  circular  insanities;  and 
the  others  were  isolated  examples  of  sundry  psychoses. 
Rydlewski,  in  twenty-nine  cases,  saw  paranoiac  psy- 
choses thirteen  times;  mania,  four  times;  manic-depres- 
sive insanity  thrice ;  hypochondria  and  melancholia  twice ; 
together  with  seven  other  forms  of  mental  disturbances. 
Of  Henderson's  five  tabetics,  two  suffered  from  hallu- 
cinatory conditions;  and  three  from  depression.  Meyer 
states  that  there  is  nothing  peculiar  or  characteristic  in 
these  psychoses.  I  think  he  errs.  Psychoses  may  acci- 
dentally complicate  tabes  as  they  may  complicate  any 
disease.  But  the  most  frequent,  the  typical  psychosis  of 
tabes,  is  an  aggravation  of  the  mental  state  induced  by 
the  tabetic  symptoms  and  habitually  present  in  tabes; 
thus,  the  depression  may  be  aggravated  to  a  persistent 
hypochondriasis ;  fear  may  breed  an  anxiety  neurosis; 
and  living  with  deceptive  sensory  intelligence  may  lead 
to  hallucinatory  and  to  delusional  insanity. 

I  have  seen  two  tabetics  under  restraint  showing  no 
memory  loss,  nor  other  symptoms  suggestive  of  general 
paresis,  but  delusions  of  hearing,  extreme  perturbation, 
fear  of  approach  and  of  unseen  influences;  phases  of 
restlessness  alternating  with  periods  of  depression  and 
with,  in  one  case,  catatonia.  This  psychosis  strongly  re- 


THE  MENTAL  STATE  OF  TABES 


179 


sembles  that  seen  sometimes  in  the  deaf  and  in  prison- 
ers undergoing  solitary  confinement. 

We  cannot  measure  the  abnormality  of  the  mental 
state  for  we  have  no  standard  of  the  patient's  normal 
average.  But  from  comparing  his  alleged  former  with 
his  present  business  and  social  capacity,  we  judge  the 
extent  of  his  deterioration ;  and  we  can  measure  his  pres- 
ent capacity  for  simple  mental  operations  such  as  mem- 
orizing, counting,  choosing,  perceiving,  associating,  etc. 
A  number  of  tests  should  be  made  so  as  to  insure  that 


FIG.  67. — The  reckoning  test:  Average  curve  of  seven  university  graduates, 
showing  from  minute  to  minute  the  percentage  variation  from  the  average 
rate  per  minute  on  the  third  day  of  the  test.  The  average  total  number  of 
additions  for  the  fifteen  minutes  was  951. 

transient  conditions  of  freshness,  fatigue,  interest,  bore- 
dom, novice-ship  and  practice  will  not  mislead  us.  The 
average  of  all  phases  of  mental  activity  thus  obtained 
affords  a  useful  standard  by  which  progress  may  be 
judged. 

I  have  examined  the  capacity  for  slight  mental  work 
in  thirty  tabetics  by  means  of  the  reckoning  test.1  The 
reckoning  test  I  used  is  a  modification  of  that  devised  by 
Oehren,  and  so  brilliantly  utilized  by  Kraepelin  and  his 
school.  It  consists  of  a  book,  resembling  the  familiar 
school  copy  book,  every  page  of  which  contains  digits, 
arranged  in  parallel  vertical  columns.  The  space  be- 
tween every  two  successive  digits  in  a  column  is  equal; 

1  Obtainable  from  the  Journal  of  Nervous  and  Mental  Diseases,  64 
AVest  56th  St.,  New  York  City. 


180 


between  adjacent  columns  an  uniform  interval  exists; 
and  the  margins  are  of  adequate  width.  Every  page  has 
ten  columns,  each  of  twenty  digits.  The  changes  which 
I  made  in  the  arrangement  of  the  text  rendered  the  ease 
of  writing  as  constant  as  possible  throughout  the  page 
and  enabled  the  number  of  pairs  added  to  be  readily 
ascertained.  To  economize  space  and  gently  to  com- 
plicate the  task,  the  digits  are  added  in  pairs  continu- 
ously; i.  e.,  after  a  pair  of  digits  has  yielded  a  sum,  the 


FIG.  68. — The  reckoning  test  of  A.  R.,  tabetic.  Curve  showing  percentage 
variation  of  work  done  from  minute  to  minute  on  third  day  of  test.  Note 
the  height  of  the  initial  spurt,  the  rapid  f ailing  off,  the  fluctuations  from  the 
fifth  to  the  ninth  minutes,  and  the  subsequent  fatigue.  Marked  fluctuations 
and  early  fatigue  are  due  mainly  to  attention  defects.  Total  output  in 
fifteen  minutes  521. 

second  digit  of  the  pair  is  linked  with  the  succeeding  fig- 
ure in  the  column,  to  form  a  new  pair.  Each  digit  (ex- 
cepting the  first  in  the  first  column)  is  thus  used  twice, 
for  the  last  digit  of  one  column  is  paired  writh  the  first 
of  the  next.  Twenty  sums  are  therefore  obtained  from 
ever^-  column  of  twenty  digits. 

The  test  is  conducted  as  follows:     The  person  to  be 
tested  is  instructed  in  the  method  of  continuous  addition. 


181 


A  few  seconds  '  warning  is  given  :  then  the  signal  to  start. 
The  person  adds  the  digits  in  pairs  as  rapidly  as  he  can. 
At  the  end  of  each  minute  the  examining  physician  calls 
"Stroke";  the  person  at  once  makes  a  mark  under  the 
last  sum  he  has  written  and  proceeds  immediately  with 
the  addition.  By  counting  the  sums  between  the  marks, 
one  can  ascertain  how  many  acts  of  addition,  how  many 


FIG.  69. — The  reckoning  test  of  J.  H.,  tabetic.  Curve  showing  percentage 
variation  of  work  done  from  minute  to  minute  on  the  third  day  of  the  test. 
Note  the  complete  absence  of  the  initial  spurt,  the  sudden  fluctuations, 
and  the  sustained  increase  in  the  last  three  minutes.  This  patient  was 
•  only  slightly  ataxic  but  was  so  frightened  that  he  would  scarcely  trust 
himself  to  move  alone.  Total  work  done  in  fifteen  minutes,  328  additions. 

units  of  mental  work,  are  done  in  each  minute.     The  test 
continues  for  fifteen  minutes. 

After  the  test  the  total  number  of  sums  is  estimated 
and  the  curve  of  the  work  from  minute  to  minute  is 
plotted  on  a  sheet  of  ruled  paper,  by  marking  the  min- 
utes along  the  abscissa  and  by  grading  the  ordinate  ac- 
cording to  the  range  of  the  number  of  sums  per  minute. 
On  such  a  curve  the  initial  spurt;  the  incidence,  height 
and  duration  of  the  maximum  working  capacity ;  the  time 
required  for  the  attainment  of  the  average  working  ca- 
pacity; the  onset  and  the  rapidity  of  development  of  fa- 
tigue; lapses  of  attention;  and  the  terminal  spurt  may 
be  observed. 


182  LOCOMOTOR  ATAXIA 

The  results  varied.  Eight  showed  no  detectable  depar- 
ture from  normal.  The  others  showed  in  varying 
degrees  the  efforts  of  fatigue  and  of  diminished  atten- 
tion. The  usual  initial  spurt  was  low  and  was  quickly 
over,  the  maximum  output  was  small,  the  work  done  from 
minute  to  minute  varied  considerably  and  tended  to  de- 
crease steadily  and  the  normal  terminal  spurt  was  not 
marked;  the  total  output  was  subnormal.  All  of  the  in- 
vestigated, except  three,  showed  a  considerable  power  of 
improvement;  indeed,  in  eleven  cases  the  improvement 
between  the  first  and  fifth  tests  exceeded  two  hundred 
per  cent. 

Because  of  this  fatigue,  attention  is  difficult  to  focus 
and  quickly  tires.  This  weakening  of  attention  gives 
rise  sometimes  to  sensory  disturbances  in  tabetics  similar 
to  those  seen  in  hysterics.  Anesthesia  may  occur  in 
bands  or  patches.  If  a  ring  be  made  round  one  of  these 
anesthetic  patches,  the  patch  on  subsequent  testing 
may  be  found  normal.  More  frequently  the  variability 
of  attention  is  disclosed  by  pronounced  oscillation  in 
the  sensory  threshold  at  the  same  site  at  different  peri- 
ods. Similarly  in  testing  vision,  I  have  observed  a  tabe- 
tic one  day  give  a  majority  of  false  responses  when  ex- 
amined with  a  32  candle-power  light;  another  day  give 
84  per  cent  of  correct  answers  when  tested  with  a  4 
candle-power  light.  If  a  slight  resistance  be  opposed  to 
abduction  or  adduction  of  the  thigh,  the  tabetic  some- 
times either  frankly  ceases  the  attempt  to  move,  or  shows 
evidence  in  his  facial  expression  of  strenuous  effort  with- 
out any  commensurate  increase  of  force  appearing  in 
the  movement.  Indeed,  palpation  may  detect  no  in- 
creased action  in  the  muscle  group  which  is  being  re- 
sisted. I  have  occasionally  been  able  to  support  on  one 


THE  MENTAL  STATE  OF  TABES          183 

finger  the  downward  thrust  of  the  heel  of  a  seated  mus- 
cular tabetic.  Further  emphasizing  the  functional  na- 
ture of  this  muscular  weakness,  is  the  astounding  gain 
in  power  which  may  be  acquired  by  a  short  training  in 
moving  against  resistance. 

The  mental  stress  of  living  with  tabes  varies  from  time 
to  time  according  to  changes  in  circumstances,  favorably 
with  rest  and  reassurance  and  in  remissions  of  pains  and 
crises,  unfavorably  in  fatigue  and  in  suffering.  But 
during  the  course  of  the  disease  the  average  daily  mental 
state  tends  gradually  to  deteriorate. 

The  rate  of  this  deterioration  is  determined  by  the 
cerebral  power  which  is  itself  dependent  upon  biological, 
environmental  and  nutritional  conditions;  by  the  extent 
and  rapidity  of  development  of  the  lesions;  and  by  the 
conditions  under  which  the  tabetic  lives.  The  chief  of 
these  conditions  is  the  amount  of  mental  strain  to  which 
he  is  daily  subject.  He  finds  he  must  exert  greater  and 
greater  efforts  to  accomplish  ordinary  business  and  so- 
cial tasks.  His  efforts  may  not  suffice ;  his  tasks  may  be 
badly  done.  If  of  the  leisured  classes,  the  tabetic  grad- 
ually restricts  his  activities  to  his  capacity.  If  the  tabe- 
tic be  an  employee,  he  loses  his  situation,  and,  if  impe- 
cunious, he  drifts  sooner  or  later  to  an  almshouse. 
Usually  his  incapacity  elicits  from  the  tabetic  less  resent- 
ment than  surrender.  He  does  not,  therefore,  as  a  rule, 
develop  a  psychosis,  but  gives  up  the  struggle  and  as- 
sumes a  mental  and  physical  immobility  which  is  partly 
forced  upon  him  but  is  mainly  a  defense  reaction  to  his 
disabilities.  This  mental  and  physical  immobility  is 
seen  to  a  greater  or  lesser  extent  in  many  of  the  hope- 
less, apathetic,  bedridden  tabetics,  inmates  of  hospitals 
and  institutions  for  chronic  diseases.  Tabetics  in  this 


184  LOCOMOTOR  ATAXIA 

stage  of  parsimony  of  effort,  of  lack  of  initiative,  of 
mental  and  physical  disuse,  are  popularly  but  errone- 
ously believed  to  be  paralyzed.  When  the  disease  by 
incapacitating  him  renders  daily  stress  less  than  his 
cerebral  power,  the  mental  state  may  remain  stationary 
or  may  even  improve — as  in  the  blind. 

The  tabetic  symptoms  create  the  uncertainty  which 
becomes  fear,  the  stress  which  procures  exhaustion,  the 
hopelessness  which  leads  to  surrender. 

The  effect  of  the  various  symptoms  upon  the  mental 
state  varies  not  only  with  their  intensity  but  also  with 
their  nature.  Thus  paresthesias  may  be  less  pernicious 
than  pains  or  crises ;  double  vision  more  disturbing  than 
loss  of  taste  or  smell;  ataxia  more  demoralizing  than 
blindness. 

Just  as  the  symptoms  react  on  the  mental  state,  so 
the  mental  state  reacts  on  the  symptoms.  In  favorable 
mental  states,  pains,  crises,  blindness,  deafness  and 
ataxia  are  all  diminished ;  in  unfavorable  mental  states, 
increased.  The  attitude  of  the  ataxic,  his  inappropriate 
wide  base,  his  curious  mixture  of  exaggerated  and  re- 
stricted movement,  his  rigid  maintenance  of  the  ill- 
judged  muscular  contractions  which  he  thinks  are  indis- 
pensable to  balancing,  are  largely  an  expression  of  the 
fear  and  tension  in  which  he  lives. 

The  influence  of  the  mental  state  upon  a  symptom 
varies  in  different  individuals  according  as  their  mental 
attitude.  With  equally  extensive  lesions  the  brave 
ataxic  walks,  the  timorous  is  bedridden ;  a  slight  urinary 
disorder  or  a  loss  of  sexual  power  may  in  one  tabetic 
scarcely  scratch  the  mental  surface  and  in  another  pro- 
duce intolerable  distress;  one  bears  cheerfully  slight 
dullness  of  hearing,  which  in  another  becomes  an  isolat- 


THE  MENTAL  STATE  OF  TABES          185 

ing  deafness.  The  mental  influence  varies  also  with  the 
nature  of  the  symptom.  It  predominates  in  motor  symp- 
toms, such  as  ataxia,  because  voluntary  movement  in- 
volves complex  mental  processes  which  are  subject  to 
every  mental  change.  It  is  also  of  essential  importance 
in  a  symptom  such  as  pain,  where  the  emotional  is  the 
chief  attribute.  But  it  little  influences  symptoms  such 
as  blindness  and  the  feeling  of  walking  on  a  thick  yield- 
ing surface,  symptoms  which  depend  on  a  simple  sensory 
perception  and  have  a  slight  emotional  content. 

Symptoms  are  supposed  to  differ  from  signs  in  that 
the  patient  experiences  the  former,  the  physician  dis- 
covers the  latter;  thus,  pain  is  a  symptom,  an  area  of 
sensory  loss  is  a  sign.  The  mental  state  influences  also 
the  so-called  signs.  Tendon  reflexes  which  on  mental 
"reinforcement"  increase,  may  temporarily  disappear 
during  the  exhaustion  which  follows  a  bout  of  pain  or  a 
gastric  crisis.  The  thresholds  of  perception  of  touch, 
pain,  vision  and  deafness  vary  from  moment  to  moment 
and  from  day  to  day,  in  correspondence  with  variations 
in  the  mental  state.  Postural  sense  loss  and  deafness 
may  spontaneously  improve  in  the  blind.  Indeed,  the 
postural  loss  may  be  more  a  measure  of  the  mental  state 
than  of  the  structural  changes. 

In  estimating  the  reciprocal  relations  of  the  mental 
state  and  the  tabetic  symptoms,  we  may  take  as  a  guide 
any  symptom.  We  may  use  the  degree  of  pain,  the 
variations  in  body  weight,  the  frequency  and  severity  of 
the  crises,  the  amount  of  exertion  necessary  to  induce 
fatigue,  or  other  similarly  variable  factors.  But  the 
more  objective  the  symptom  the  better  index  it  affords. 
Ataxia,  once  it  has  developed,  is  the  most  evident,  the 
easiest  to  measure  and  the  most  reliable  guide,  "and  it, 


186  LOCOMOTOR  ATAXIA 

moreover,  tends  to  displace  pains  and  crises  as  an  emo- 
tional expression. 

In  considering  the  ratio  of  the  ataxic  tendencies  to  the 
coordinating  power,  we  saw  (p.  78)  that  the  lesions  may 
be  regarded  as  a  constant,  and  the  daily  incentives  to 
fear,  anger,  excitement,  fatigue  and  depression,  as  a  vari- 
able, in  determining  the  liability  to  ataxia,  the  degree  of 
ataxia :  that  ataxia,  although  partly  a  manifestation  of 
structural  change,  is  chiefly  an  emotional  expression,  a 
phenomenon  of  the  mental  state  (p.  82) ;  that  the  tempo- 
rary aggravation  of  ataxia  which  accompanies  blindness 
is  due  to  the  concomitant  aggravation  of  the  mental  state : 
and  that  the  subsequent,  spontaneous  disappearance  of 
ataxia  arises  from  the  improvement  which  the  enforced 
reduction  of  effort  confers  upon  the  mental  state  in  the 
blind.  We  also  saw  that  the  length  of  the  preataxic  and 
of  the  ataxic  periods  was  determined  chiefly  by  the  men- 
tal state.  The  mental  state  and  this  tabetic  symptom 
are  related  as  a  mirrored  image  and  its  object. 

The  relationship  between  mental  state  and  tabetic 
symptom  implies  the  interdependence  of  the  tabetic 
symptoms.  Through  the  mental  state  a  circuit  is  estab- 
lished between  the  various  symptoms  so  that  increase  of 
one  increases  the  others  and  reduction  of  one  reduces 
the  others.  Aggravation  of  pain,  or  of  crisis,  or  of  blad- 
der, or  of  other  trouble,  aggravates  the  mental  state 
and  increases  ataxia;  amelioration  of  any  of  these  trou- 
bles improves  the  mental  state  and  diminishes  ataxia. 
Thus  psychotherapy  aimed  at  any  symptom  improves 
usually  the  others.  The  cure  of  ataxia  by  treatment  or 
through  blindness  is  accompanied  by  gain  in  weight,  in- 
creased powrer  to  sleep,  spontaneous  diminution  or  cessa- 
tion of 'pain,  and  often  by  returning  virility.  The  ex- 


THE  MENTAL  STATE  OF  TABES  187 

tent  of  the  improvement  in  coordination  depends  solely 
upon  the  amount  to  which  the  mental  state  improves. 

Under  any  treatment  in  which  one  or  more  of  his  vari- 
ous disabilities  are  alleviated,  or  in  which  the  patient  has 
faith,  the  mental  state  improves.  Hence  medicinal  sub- 
stances with  or  without  pharmacological  worth  gain  re- 
pute. Boots  and  belts,  if  sufficiently  lauded,  produce 
more  benefit  than  their  mechanical  qualities  warrant. 
Electricity,  baths,  massage,  and  other  measures  produce 
results  disproportionate  to  their  merits.  I  have  seen 
one  ataxic  who  acquired  marked  benefit  from  Christian 
Science  and  another,  from  hypnosis.  The  influence  of 
these  measures  depends  to  a  greater  or  less  degree  upon 
the  emotional  appeal  which  they  make.  Thus,  the  influ- 
ence of  drugs  upon  the  mental  state  is  usually  greater 
when  they  are  administered  by  rubbing  than  by  inges- 
tion.  The  circumstance  attending  salvarsan  injection, 
together  with  that  drug's  reputation,  is  responsible  for 
much  of  the  alleviation  of  pain,  fatigue  and  depression 
which  sometimes  follows  its  use;  and  this  psychic  effect 
is  especially  marked  after  the  rubric  which  attends  the 
intraspinal  administration  of  salvarsanized  serum.  High 
frequency  may  be  more  potent  than  less  esoteric  forms 
of  electricity,  and  electrical  applications  to  the  posterior 
urethra  may  be  more  beneficial  than  similar  applications 
to  atrophied  muscles. 

No  skilful  beginner  can  cause  the  mental  state  to  im- 
prove as  can  the  healer  of  popular  repute.  No  method 
of  treatment  when  first  tried  can  influence  the  mental 
state  so  powerfully  as  when  the  faithful  later  flock  to 
it  for  cure. 

The  value  of  any  treatment  of  the  mental  state  of 
tabetics  is  proved  not  by  samples  of  its  miraculous  power 


188  LOCOMOTOR  ATAXIA 

but  by  its  ability  to  command  success  when  administered 
by  those  who  lack  the  personality  of  its  protagonist  and 
by  its  ability  to  heal  those  of  little,  as  well  as  those  of 
much,  faith.  Any  method  which  every  medical  man  can 
successfully  use,  and  from  which  every  tabetic  shall 
derive  benefit  must  be  based  upon: — 

I.  Knowledge  of  the  mechanism  of  symptoms,  and  of 
the  relative  importance  of  the  structural  change  and  of 
the  mental  state  in  producing,  in  aggravating,  and  in  per- 
petuating every  symptom. 

II.  Knowledge    of   the   reciprocal   relations   between 
symptoms  and  the  mental  state,  and  of  the  interdepen- 
dence of  symptoms. 

III.  Knowledge   of  the   constitution,    reactions,   and 
capacity  of  the  tabetic's  psyche. 

With  this  knowledge  we  can  by  treating  the  mental 
state,  treat  the  symptom ;  and  by  treating  the  symptom, 
treat  the  mental  state. 

In  treating  the  mental  state,  we  avoid  all  circum- 
stances detrimental  to  mental  function,  all  occasions  of 
fatigue,  fear,  depression  or  other  unfavorable  reaction. 
We  procure  mental  rest  and  build  up  an  available  re- 
serve of  mental  strength.  We  train  attention  and  we 
teach  order  and  system  in  mental  action. 

In  treating  the  symptom,  we  avoid  provoking  it;  we 
minimize  it  by  mechanical  means,  such  as  braces,  in 
ataxia;  we  palliate  it  by  innocuous  doses  of  drugs,  such 
as  phenacetin,  antipyrin,  and  other  so-called  analgesics, 
in  pain ;  we  remedy  it  by  physical  therapy,  such  as  mas- 
sage, electricity  and  movement  in  muscular  weakness; 
and  so  forth. 

The  cardinal  treatment  is  the  treatment  expressly 
directed  towards  improving  the  mental  state.  When,  as 


THE  MENTAL  STATE  OF  TABES          189 

in  ataxia,  the  symptom  reflects  the  mental  state  and  the 
mental  state  is  the  chief  source  of  the  symptom,  the  treat- 
ment of  the  mental  state  and  of  the  symptom  are  uni- 
fied. 

We  shall  consider  first  the  general  principles  of  treat- 
ing the  mental  state,  and  then  the  auxiliary  symptomatic 
treatment  of  the  tabetic. 


CHAPTER  XI 

TREATMENT  OF  THE  MENTAL  STATE:  TREATMENT  OF 
THE  SYPHILITIC  NEURASTHENIC  AND  OF  THE  PRE- 
ATAXIC  TABETIC. 

Imperative  necessity  for  treatment  of  syphilitic  neurasthenia,  the  pre- 
cursor of  tabes  and  paresis.  Principles  of  treatment :  rest,  reduc- 
tion of  effort  to  capacity,  avoidance  of  harmful  thinking,  training 
in  mental  control,  freedom  from  unnecessary  medical  interference: 
Treatment  of  the  preataxic  tabetic.  Prosecution  for  syphilis. 
Communicating  the  diagnosis.  Reducing  mental  expenditure. 
Isolation  and  imprisonment.  Immobilization  and  rest.  Effect  of 
attitude  in  perpetuating  and  aggravating  stress.  The  teaching  of 
rest.  Rest  exercises,  respiratory  and  muscular.  Psychological  and 
physiological  effect  of  the  exercises;  effect  on  blood  pressure,  pulse 
rate  and  pulse  rhythm.  Exercises  in  controlling  mental  processes 
through  movement.  Respiratory  exercises,  pneumograph.  Head 
exercises,  cephalograph.  Eye  exercises.  Exercises  in  mental  work. 
The  reckoning  test.  The  daily  schedule.  Results  and  duration  of 
regime.  The  transition  period.  The  return  to  business  and  social 
life.  Systematizing  and  limiting  daily  effort.  Importance  of  prac- 
ticing the  exercises  to  prevent  relapses  and  to  avoid  ataxia. 

ALTHOUGH  a  virulent  spirochete  may  bring  tabes  to 
anyone,  a  non-virulent,  we  have  stated  (page  149),  may 
make  the  nervous  a  tabetic  or  a  paretic.  As  the  nervous 
syphilitic  is  a  potential  tabetic,  a  potential  general  pare- 
tic, he,  of  all  neurasthenics,  imperatively  requires  unre- 
mitting care. 

Syphilitics  often  complain  of  irritability;  of  the  in- 
creasing readiness  with  which  they  experience  fatigue; 
of  tumultuous  and  irregular  heart  action ;  of  lack  of  appe- 
tite, hyperacidity  and  nausea ;  and  of  constipation  punc- 
tuated by  diarrhea.  These  symptoms,  common  to  states 
of  mental  stress,  are  due  to  increased  tone  of  the  vagus 

190 


TREATMENT  OF  MENTAL  STATE          191 

and  may  be  alleviated  by  a  drug  which  reduces  vagal 
tone,  such  as  atropin. 

But  incomparably  better  than  the  palliative  treatment 
of  symptoms  by  drugs  is  the  care  of  the  mental  state. 
The  essence  of  that  care  is  rest. 

I  lately  treated  a  syphilitic  in  whom  business  tension 
due  to  the  war  caused  a  nervous  breakdown,  a  cardiac 
neurosis  with  fear  and  sleeplessness.  His  devoted  wife 
insisted  upon  nursing  him:  she  quickly  tired,  and  devel- 
oped optic  atrophy. 

A  necessary  preliminary  to  rest  is  a  careful  examina- 
tion of  all  of  the  neurasthenic's  difficulties.  The  more 
thoroughly  his  problems  and  his  reactions  to  them  are 
investigated,  the  more  successfully  can  he  be  aided.  This 
investigation  permits  the  reduction  of  the  patient's 
effort  to  his  capacity.  It  also  affords  opportunities  to 
explain  distressing  reactions  and  to  warn  the  neuras- 
thenic against  injurious  thinking. 

The  neurasthenic  should  also  be  taught  to  control  his 
mental  processes,  to  think  correctly.  In  such  teaching,  a 
beginning  should  be  made  with  a  task  within  his  mental 
reach,  a  task  which  is  part  of  his  every  day  experience. 
It  must  require  no  new  perception,  no  new  mechanisms, 
no  elusive  interpretations.  The  mental  processes  in- 
volved in  the  task  must  have  an  outward  equivalent  by 
which  their  action  may  be  judged,  corrected,  perfected. 
The  mental  processes  which  we  can  best  externalize  are 
those  which  have  a  measurable  motor  result. 

Training  of  mental  processes  is,  therefore,  procured 
through  training  in  movement.  We  desire  a  posture :  its 
attempted  attainment  follows.  We  judge  how  the  per- 
formance fulfills  the  desire.  By  repeated  effort,  we  train 
ourselves  to  make  the  movement  mirror  the  desire:  the 


192  LOCOMOTOR  ATAXIA 

act  becomes  effortless.  From  simple,  complex  movements 
are  reached,  all  accurately  performed  and  repeated  in 
carefully  regulated  doses. 

The  effect  of  this  training  is  not  confined  to  the  sphere 
of  movement  wherein  it  is  gained.  It  influences  for  good 
all  mental  effort.  It  improves  all  mental  activities.  It 
inculcates  the  art  of  attending,  of  sustained  effort,  of 
logical  sequence,  of  mental  control. 

The  treatment  of  the  syphilitic  neurasthenic  consists 
in  these  measures :  it  consists  also  in  freedom  from  pros- 
ecution for  syphilis :  in  freedom  from  depression  by  mas- 
sive doses  of  mercury  or  arsenic;  and  in  freedom  from 
repeated  examination  of  the  cerebrospinal  fluid.  Heroic 
treatment,  and  over-zealous  investigations,  of  non-essen- 
tial attributes  of  syphilitic  disease  in  the  central  nervous 
system,  undoubtedly  harm  the  neurasthenic.  Variations 
in  the  cell-count,  in  the  globulin  content,  and  in  the  Was- 
sermann  reaction  of  the  cerebrospinal  fluid  are  often 
of  less  interest  to  him  than  to  the  serologist. 

The  beneficent  effect  of  psychotherapy  upon  the  course 
of  the  syphilitic  invasion  called  tabes  contains  the  prom- 
ise that  the  intelligent  care  of  the  syphilitic  neurasthenic 
may  be  powerful  to  retard  that  invasion. 

The  treatment  of  the  preataxic  tabetic  does  not  differ 
in  any  essential  particular  from  that  of  the  syphilitic 
neurasthenic. 

Some  tabetics  are  ignorant  of,  but  most  suspect  the 
syphilitic  origin  of  their  trouble.  Experiencing  the  re- 
lentless consequences  of  a  long  past  accident,  the  tabetic 
dreads  the  future  not  only  for  himself  but  for  his  fam- 
ily. In  1909,  a  young,  married,  preataxic  tabetic,  dis- 
tressed for  two  years  by  a  baffling  pain  in  his  legs,  went 
with  his  father,  a  clergyman,  to  consult  a  knighted  neu- 


193 

rologist  of  popular  repute.  After  discovering  absent 
knee-jerks,  the  knight  impressively  said  to  the  tabetic, ' '  I 
am  now  going  to  ask  you  a  question  which  it  would  be 
equally  my  duty  to  put  to  the  Archbishop  of  Canterbury, 
were  he  in  your  condition.  Have  you  ever  had  syphilis  ? ' ' 
The  tabetic  denied  infection  but  was  forced  to  admit,  be- 
fore his  horrified  father,  that  he  had  been  exposed  to  the 
risk.  The  immediate  scene  and  the  subsequent  estrange- 
ment of  his  family  speedily  resulted  in  severe  ataxia,  for 
which  he  was  treated  at  the  National  Hospital,  London, 
where  I  then  was  House  Physician. 

A  discreet  blood  examination  is  more  authoritative 
and  more  frank  than  the  most  minutely  extracted  con- 
fession. Other  data  regarding  the  infection  and  the 
family  health  may  be  obtained  from  the  family  physician 
or,  later,  by  tactful  questioning,  without  startling  him  or 
confirming  his  fears,  from  the  patient  himself.  Accord- 
ing to  our  present  knowledge  of  tabes,  the  influence  which 
most  often  makes  the  syphilitic  develop  tabes  is  mental 
stress.  Mental  stress  results  from  overwork.  Over- 
work is  to  a  civilian  as  honorable  a  cause  of  unfitness  as 
a  bullet  is  to  a  soldier.  And  there  is  great  mental  ease 
in  an  honorable  cause.  The  incrimination  of  overwork 
is  not  only  humane,  it  is  just ;  and  it  is  the  only  basis  of 
successful  treatment  of  tabes. 

There  still  attaches  to  tabes  much  of  the  pessimism  of 
sixty  years  ago  when  German  neurologists  taught 
"Ueber  alle  ist  der  Stab  gebrochen."  I  have  already 
mentioned  my  knowledge  of  two  physicians,  afflicted  with 
tabes,  committing  suicide.  A  tabetic  whom  I  have  twice 
demonstrated,  and  who  was  formerly  a  medical  student, 
six  years  ago  consulted  a  doctor  for  intermittent  pain 
in  the  stomach,  accompanied  by  vomiting,  and  having  no 


194  LOCOMOTOR  ATAXIA 

relation  to  food.  He  next  had  transient  double  vision. 
Three  years  later  sudden  pains  in  his  legs  appeared, 
which  another  doctor  called  rheumatic.  He  visited  a 
third  doctor  a  year  afterwards  who,  for  the  first  time, 
associated  the  word  "shooting"  with  the  pain.  There 
arose  in  the  patient's  memory  a  medical  tag  twenty  years 
old,  and  he  asked  if  " shooting  pains"  were  not  typical 
of  locomotor  ataxia.  The  doctor  agreed  that  they  were. 
''Have  I  locomotor  ataxia?"  "I"  don't  know,  I  am  no 
nerve  specialist."  The  patient  who  had  entered  walk- 
ing well,  now  greatly  perturbed,  with  much  difficulty 
reeled  home.  He  was  literally  staggered  by  the  suspi- 
cion that  he  had  the  much  dreaded  disease.  Ataxia 
thereafter  swiftly  incapacitated  him.  His  power  to  walk 
correctly  had  survived  unimpaired  through  five  years 
of  his  malady.  A  correct  diagnosis  was  more  pernicious 
to  him  in  its  immediate  effects  than  five  years  of  mis- 
taken therapy. 

When  characteristic  symptoms  arise,  too  great  tact 
cannot  be  shown  in  dealing  with  the  incipient  tabetic. 
The  diagnosis  may  be  communicated  to  the  family  physi- 
cian :  the  last  to  hear  it  should  be  the  patient  or  his  f am- 
ily. 

The  first  step  in  treating  the  preataxic  tabetic  is  to 
reduce  the  expenditure  of  mental  energy  below  the 
income.  By  progressively  reducing  effort,  we  may 
attain  the  level  where  a  saving  margin  is  daily  attained. 
Usually,  we  institute  a  sudden  rigid  economy  of  effort 
by  interrupting  all  social  and  business  activity. 

In  reducing  expenditure  of  mental  energy,  we  do  not 
merely  isolate  the  patient  with  his  worries.  Prisoners 
in  solitary  confinement  are  more  likely  to  go  mad  than 
to  acquire  tranquillity.  Neither  do  we  merely  immobilize 


TREATMENT  OF  MENTAL  STATE          195 

him  and  call  it  rest.  Many  tabetics  have  been  so  rested 
who  have  never  walked  properly  again. 

To  remove  a  patient  from  his  problems  is  not  to  solve 
them.  He  carries  their  burden  with  him,  a  burden  which 
the  physician  must  at  least  share.  Sympathetic  atten- 
tion, careful  inquiry,  experienced  interpretation  and 
advice,  and,  above  all,  systematic  reassurance  are  neces- 
sary to  bring  ease  to  the  preataxic  tabetic.  Even  with 
such  aid,  given  diligently,  the  tabetic  in  his  pain  and  anx- 
iety can  often  neither  sleep  nor  rest  adequately.  He 
must  be  taught  to  rest. 

According  to  James,  we  are  ashamed  because  we  blush, 
we  fear  because  we  tremble,  we  are  pleased  because  we 
laugh.  Without  the  blush  we  would  feel  no  shame; 
without  the  trembling,  no  fear;  without  the  laughter,  no 
joy.  Sherrington,  after  testing  James'  theory,  con- 
cludes : 

' '  In  view  of  these  general  considerations  and  of  the  above  ex- 
periments, we  may  with  James  accept  visceral  and  organic  sen- 
sations and  the  memories  and  associations  of  them  as  contribu- 
tory to  primitive  emotions  but  we  must  regard  them  as  rein- 
forcing rather  than  irritating  the  psychosis.  Organic  and  vascu- 
lar reaction,  though  not  the  actual  excitant  of  emotion,  strength- 
ens it.  This  is  the  kernel  of  the  old  contention  about  the  actu- 
ality of  emotion  in  the  art  of  the  artist.  Hamlet 's  description  of 
an  artist  as  really  moved  by  his  expression  may  be  accepted  as 
an  answer"  (The  Integrative  Action  of  the  Nervous  System, 
pp.  267-268). 

The  attitude  of  the  tabetic  is  an  expression  and  a  cause 
of  the  tension  in  which  he  lives.  The  attitude  is  mus- 
cular with  cardiovascular  and  respiratory  accompani- 
ments. The  removal  of  that  expression  relieves  his 
mental  tension.  To  remove  it,  I  devised  the  following 
rest  exercises: 


196 


LOCOMOTOR  ATAXIA 


The  tabetic  is  instructed  to  breathe  deeply  and  to  pause 
at  the  end  of  inspiration  and  of  expiration. 

Having  thus  f  ocussed  his  attention,  he  passes  to  breath- 
ing of  moderate  amplitude.  The  breathing  is  abdominal 
in  type,  slow  in  rate,  and  uniform  in  rhythm.  The 
tabetic  stops  distracting  thoughts  as  they  arise,  and  de- 


FIG.  70. — Description  of  parts  as  numbered  on  drawing  of  chest  piece  of 
pneumograph:  1,  Breast  plate  lined  with  leather  pad  on  concave  surface. 
2,  Fulcrum  plate  showing  mode  of  attachment  to  breast  plate.  S,  Fixation 
plate.  4,  Diaphragm  or  metal  tambour.  5,  Outlet  and  hose  connection 
to  diaphragm.  6,  Rubber  hose  connecting  chest  piece  to  recording  ap- 
paratus. 7,  Tension  adjustment  rod  and  nut.  8,  Metal  protecting  cover 
over  diaphragm.  9,  Silk  belt  around  chest.  10,  Belt  clamp  for  adjust- 
ing free  end  of  silk  belt  to  breast  plate.  11,  Ribbon  suspending  chest 
piece  around  the  neck. 

votes  his  attention  solely  to  the  sensations  which  accom- 
pany his  breathing.  A  bag  of  sand  or  shot,  or  the  physi- 
cian's  hand,  placed  upon  the  abdomen,  increases  the  mus- 
cular effort  so  that  the  breathing  may  not  easily  lapse 
into  an  unconscious  act.  After  moderate,  gentle  breath- 
ing is  practised. 


o 

S    aw^ 


197 


198 


LOCOMOTOE  ATAXIA 


Then,  muscular  flaccidity  is  procured.  Every  limb  is 
dealt  with  separately.  Every  joint  is  passively  moved 
in  turn.  The  muscles  are  first  stretched  slowly  and 
steadily  and  next  are  similarly  relaxed.  When  the  pre- 
vailing muscular  tension  has  thus  been  passively  re- 
moved, the  joints  are  free  from  muscular  constraint ;  the 

P 


FIG.  72. — Up  strokes  represent  inspiration,  down  strokes  expiration. — Types 
of  breathing  disturbance.  Note  that  inspiration,  instead  of  being  a  con- 
tinuous act,  is  performed  in  two  or  more  parts.  Expiration,  the  pause 
between  inspiration  and  expiration, 'and  as  a  rule,  the  pause  between 
expiration  and  inspiration  are  here  relatively  unaffected.  P  indicates 
pause. 

limbs  lie  flaccid  and  motionless ;  and  fall  limply  from  any 
unsupported  position. 

The  scalp,  forehead,  cheek  and  jawT  muscles  of  the 
recumbent  patient  are  passively  moved,  till  wrinkling 
diminishes  or  disappears,  and  muscular  twitching  ceases. 
After  procuring  flaccidity  in  the  muscles  of  the  first  limb, 
the  physician  turns  again  to  the  scalp,  forehead,  cheeks, 
and  jaw;  relaxes  those,  and  then  again  the  limb.  This 
linking  of  parts  previously,  to  parts  newly,  freed  from 


TREATMENT  OF  MENTAL  STATE 


199 


muscular  constraint,  is 
helpful  in  bringing  the 
whole  to  a  satisfactory 
state  of  flaccidity. 

The  relaxation  of  the 
neck  and  trunk  muscles 
is  best  accomplished 
while  the  patient  sits. 
The  patient 's  arms 
should  then  hang  limply 
by  his  side,  and  his  feet, 
crossed  one  over  the 
other,  should  rest  on 
their  outer  borders. 
The  head  should  next  be 
passively  rotated  in  all 
directions,  slowly  and 
repeatedly.  Then,  by 
moving  the  supported 
trunk,  the  head  is  al- 
lowed to  fall  passively 
backward  and  forward, 
by  its  own  weight.  Fi- 
nally, the  head  rests 
with  the  chin  upon  the 
chest,  or  hangs  forward 
suspended  by  the  liga- 
ments of  the  neck. 

The  trunk  should  be 
slowly  bent  backward 
and  forward  and  from 
side  to  side,  until  suffi- 
cient loosening  of  the 


200 


LOCOMOTOR  ATAXIA 


muscles  is  obtained  to  allow  the  trunk  to  gravitate  with- 
out restraint  in  whatever  direction  it  is  inclined,  un- 
supported. 
All  movements  should  be  passively  made  by  the  physi- 


FIG.  74. — Types  of  breathing  disturbances.    Contrast  the  slowness  and  irregu- 
larity of  inspiration,  which  is  consciously  performed,  with  the  speed  and 

uniformity  of  expiration,  which  occurs  automatically.    P  indicates  pause. 

• 

cian,  and  then,  if  possible,  passively  induced  by  the  ac- 
tion of  gravity. 

Besides  the  tranquilizing  of  excited  and  anxious  men- 
tal states  and  the  removal  of  constraint  from  the  muscu- 


FIG.  75. — Patient  A.,  Curve  A. — Types  of  breathing  disturbance.  Jerkiness 
pervades  the  whole  act,  producing  a  staircase  curve.  The  series  of  jerks 
and  halts  show  that  the  muscles  of  respiration  may  produce  chest  move- 
ments analogous  to  the  ataxic  movements  we  observe  in  limbs.  The 
following  six  curves  show  the  gradual  acquiring  of  respiratory  control  by 
the  patient  A. 


lature,  certain  other  physiological  effects  result  from 
these  exercises.  A  reduction  of  25  to  30  mm.  in  high 
blood  pressures  commonly  occurs.  The  reduction  is  not 
confined  to  high  blood  pressures :  a  fall  of  10  to  15  mm. 


TREATMENT  OF  MENTAL  STATE 


201 


happens  in  blood  pressures 
which    are    nearly    normal. 
As   a  rule,   in   normal  and 
sometimes  also  in  abnormal 
pressures,  the  fall  affects  the 
systolic  and  diastolic  pres- 
sures equally;  but  in  abnor- 
mally   high    pressures,    the 
systolic  usually   falls   more 
than  the  diastolic.    In  cases 
in  which  high  blood  pressure 
is   not    due    to    cardiorenal 
disease,  the  diastolic  some- 
times  falls   lower   than  the 
systolic.      Indeed,    in    such 
cases,  a  fall  is  not  invari- 
able :  a  rise  may  occasionally 
occur,    particularly    in    the 
diastolic  pressure.    Whether 
the  blood  pressure  be  low- 
ered or  raised  by  the  exer- 
cises, the  pulse  pressure  ra- 
tio, if  abnormal,  tends  to  ap- 
proximate to  normal. 

Besides  the  fall  of  blood 
pressure,  a  decrease  in  the 
pulse  rate,  though  sometimes 
slight,  and  rarely  absent,  as 
a  rule  is  very  evident.  Some- 
times the  pulse  rate  falls 
thirty  or  forty  beats  a  min- 
ute, usually  ten  to  fifteen. 
The  higher  the  initial  pulse 


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202 


LOCOMOTOR  ATAXIA 


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rate,  the  greater  is  the  lowering. 
Besides  the  decrease  in  the  pulse 
rate,  pulse  irregularities  dimin- 
ish or  disappear  during  the  exer- 
cises. Not  only  is  rhythm  re- 
stored but  the  pulse  volume  tends 
to  become  uniform. 

Psychologically,  these  exercises 
produce  concentration  of  atten- 
tion. The  physiological  effects 
are  relaxation  of  the  voluntary 
muscles,  diminution  of  muscular 
reflexes,  slowing  of  the  pulse  rate, 
reestablishment  of  uniformity  in 
the  rhythm  and  volume  of  the 
pulse,  lowering  of  blood  pressure 
and  restoration  of  the  normal 
pulse-pressure  ratio. 

As  a  routine  procedure,  the 
tabetic  is  instructed  simply  and 
briefly  in  the  essentials  of  the  ex- 
ercises. Then,  in  a  quiet  room, 
he  lies  on  a  couch  sufficiently  high 
to  enable  the  physician  to  work 
without  stooping  unduly,  and  suf- 
ficiently broad  to  prevent  the 
limbs  from  falling  over  the  edge. 
The  tabetic's  head  rests  on  a  low 
and  not  too  soft  pillow.  He  is 
now  told  to  breathe  deeply.  From 
deep  breathing  he  passes  to  me- 
dium, and  finally  to  gentle  breath- 
ing. Then  muscular  relaxation  is 


203 

systematically  procured  by  passive  movements,  begin- 
ning with  the  face  and  limbs,  and  proceeding  to  the  head 
and  trunk.  Throughout  the  passive  movements,  the  phy- 
sician periodically  corrects  the  breathing,  slows  it  as  it 
quickens,  insures  adequate  pauses  at  the  end  of  inspira- 
tion and  expiration,  and  encourages  rhythmic,  not  stac- 
cato movements. 

The  objective  guide  to  success  is  the  behavior  of  the 
eyelids.  When  the  lids  are  still,  the  pulse  rate  has 
slowed,  and  the  blood  pressure  has  fallen;  when  quiver- 
ing returns,  the  tabetic  is  uncomfortable  or  distracted, 
and  the  pulse  rate  and  the  blood  pressure  have  increased. 
By  watching  the  eyelids,  we  can  guess  the  progress,  and 
we  need  not  disturb  the  patient  by  frequent  pulse  or 
pressure  observations. 

The  training  usually  begins  with  several  ten  minute 
exercises,  separated  by  short  intervals.  As  the  tabetic 
learns,  the  exercises  may  be  lengthened  to  three  quarters 
of  an  hour.  Five  or  ten  lessons  usually  suffice  to  teach 
the  whole  procedure. 

The  easier  he  is  to  teach  the  less  is  the  strain  upon 
him,  and  the  more  pronounced  is  the  relief  of  his  muscu- 
lar, vascular,  and  mental  tension. 

Most  nervously  exhausted  tabetics  have  lost  weight. 
They  must,  therefore,  be  fed  with  quantities  sufficient  not 
only  to  maintain  life,  to  replace  the  daily  cellular  waste, 
but  also  to  repair  outstanding  tissue  destruction.  It  is 
the  amount  absorbed,  not  the  amount  ingested  which 
counts.  Meals  should  be  frequent,  ample,  not  exces- 
sive, daintily  served,  appetizing  and  easily  digested. 
The  elimination  of  waste  products  may  need  regula- 
tion. 


204 


LOCOMOTOK  ATAXIA 


8 
I 


6 


As  useful  adjuvants  to  stabiliz- 
ing the  vascular  and,  through  it,  the 
mental  tension,  cold  baths  are  valu- 
able. For  those  who  react  badly, 
first,  cold  sponging  and  drying  of 
the  body  in  sections ;  next,  envelop- 
•  ment  in  a  cold  wet  sheet  accom- 
panied by  friction ;  then,  high  pres- 
sure douches  for  gradually  length- 
ening periods  at  progressively  low- 
er temperatures,  and  finally  alter- 
nating hot  and  cold  douches,  may 
be  necessary  as  a  training  for  cold 
baths. 

The  tabetic  trained  to  rest  is  en- 
dowed with  the  necessary  prelimi- 
nary to  all  effort,  the  power  to  re- 
cuperate. Treatment  must  now  be 
directed  towards  training  his  cere- 
bral control.  I  begin  with  breath- 
ing exercises,  for  breathing  is  not 
arduous  and  it  exerts  a  powerful 
influence  not  only  over  mental  but 
also,  as  we  have  seen,  over  visceral 
functions.  To  use  breathing  as  an 
exercise  in  control  requires  no  ap- 
paratus. The  method  already  out- 
lined may  suffice.  But  by  graphi- 
cally and  visibly  recording  breath- 
ing by  a  pneumograph x  such  as 
Knauer  and  Maloney  devised,  the 

1  Made  by   the  Medical  Machinery   Com- 
pany, Detroit. 


TEEATMENT  OF  MENTAL  STATE 


205 


respiratory  movements  may  be  imme- 
diately seen  and  any  deviation  from 
the  normal,  at  once  appreciated, 
checked,  and  corrected.  Practice  in- 
sures greater  and  greater  control, 
more  and  more  perfect  breathing.  At 
first  at  a  slow,  then  at  the  normal, 
rate ;  at  first  sustained  only  for  a  short 
time,  later  for  longer  and  longer  pe- 
riods; at  first  in  quietness,  and  then 
with  measured  distraction,  orderly 
breathing  is  attained.  Later  exercises 
comprise  regularly  recurring  altera- 
tions in  the  duration  of  inspiration,  of 
expiration  and  of  the  pauses  between 
them,  timed  by  the  metronome.  The 
mental  state  so  far  as  it  is  reflected  in 
the  most  delicate  of  all  indices,  respi- 
ration, becomes  a  matter  of  record,  a 
source  of  reassurance  and  encourage- 
ment to  both  patient  and  physician. 
To  obviate  swaying  (Rombergism), 
to  insure  equilibration,  and  fur- 
ther to  train  the  mental  processes  in 
ordered  action,  exercises  in  main- 
taining the  head  steady  and  in  con- 
trolling head  movements  may  be  prac- 
tised with  the  cephalogi  aph.  Tn  every 
plane  movements  of  regulated  extent 
and  rate  may  be  performed.  As 
the  slightest  movement  is  immedi- 
ately recorded  by  the  writing  point, 
the  patient  can  see  any  errors  as 


f 


206 


LOCOMOTOR  ATAXIA 


they  occur  and  may  forthwith  control  and  correct  them. 
Training  in  eye  movements  is  also  valuable.  Every 
movement  should  be  of  prescribed  direction,  extent  and 
rate.  In  such  training  a  perimeter  with  a  movable  car- 
riage may  be  used.  The  carriage  bears  a  frame  fixed  by 


FIG.  80. — Curve  A  6. — Next,  still  deeper  respirations  are  practised.  P  =  pause. 

a  central  pivot  on  which  it  can  rotate.  The  frame  holds 
two  mirrors,  the  distance  between  which  can  be  changed. 
Maintaining  the  head  immovable,  the  patient  sees  the 


FIG.  81. — Curve  A  7. — Then,  slow  deep  breathing  is  taught.  And  the  exer- 
cises are  continued  and  varied  until  the  patient  acquires  complete  control 
over  respiration. 

image  of,  say,  his  right  eye  in  a  mirror  at  the  fixation 
point.  The  mirror  is  then  steadily  moved  in  one  direc- 
tion for  a  certain  distance,  at  a  constant  rate.  So  long 
as  the  patient  looks  in  the  mirror,  his  eye  moves  only  in 
accordance  with  the  movement  of  the  mirror.  If  the 


TREATMENT  OF  MENTAL  STATE          207 

mirror  moves  beyond  his  range,  he  loses  sight  of  the  mir- 
rored image.  The  eyes  should  be  exercised  in  all  direc- 
tions; at  first,  singly,  then  conjointly;  at  first  slowly,  then 
more  rapidly.  Through  the  aid  of  such  movements  the 
squints  and  diplopia  of  tabes  disappear  in  an  astonishing 
manner. 

Besides  respiratory,  head,  and  eye  movements,  other 
^luscular  exercises  are  of  great  value.  These  will  be 
more  fully  described  when  we  consider  the  treatment  of 
the  ataxic.  All  movements  must  be  accurately  defined, 
precisely  performed,  and  carefully  regulated  in  their 
time  relations  by  means  of  the  metronome. 

The  reckoning  test  is  also  of  great  value.  I  have 
already  described  (p.  180)  its  diagnostic  use.  Its  em- 
ployment periodically  for  a  few  days  affords  an  objective 
criterion  of  the  progress  of  a  morbid  mental  state.  But 
the  reckoning  test  provides  also  a  mental  task  the  dosage 
of  which  can  be  graduated  like  that  of  any  other  thera- 
peutic measure.  Patients  take  a  great  interest  in  the 
test :  the  spirit  of  emulation  is  often  astonishingly  keen 
among  them,  and  the  knowledge  of  their  daily  results 
urges  them  to  greater  efforts.  The  therapy  of  psychic 
states  cannot  but  welcome  such  a  valuable  accession  to 
its  strength. 

The  training  in  the  rest  exercises  is  itself  the  begiiL- 
ning  of  training  in  attention  and  in  sustained  and  con- 
trolled effort.  With  the  movement  exercises  or  other 
tasks,  a  gentle  beginning  must  be  made.  At  the  first  at- 
tempt a  few  minutes'  practice  is  enough.  As  soon  as  a 
pulse  rises  more  than  ten  beats  per  minute,  all  effort 
should  cease  in  favor  of  the  rest  exercises.  Soon  the 
time  spent  in  work  equals  and  then  exceeds  that  spent 
in  rest. 


FIG.  82. — Chart  of  a  patient  beginning 
test,   remarkable  improvement   in 
208 


treatment,  showing  by  the  reckoning 
her  capacity  for  simple  mental  tasks. 

209 


210  LOCOMOTOR  ATAXIA 

The  patient's  day  must  be  carefully  mapped  out.  The 
hours  of  waking,  eating,  working,  resting  and  sleeping 
must  all  be  scheduled.  Each  night  the  day's  achieve- 
ment must  be  recorded.  The  treatment  must  be  method- 
ical :  every  moment  must  be  filled ;  there  is  no  time  for 
introspection  and  worrying  in  a  properly  arranged 
course  of  psychotherapy. 

The  earliest  result  of  this  regime  is  sleep,  sometimes 
wonderfully  prolonged  and  refreshing  sleep;  then  the 
capacity  for  effort  increases,  the  weight  grows  and  ex- 
citement and  anxiety  decrease. 

This  intensive  treatment  should  %ot  last  longer  than 
its  usefulness.  If  all  results  are  charted  we  can  ascer- 
tain the  moment  progress  slows  or  halts.  The  patient 
should  then  be  transferred  with  his  nurse  to  the  country, 
where  in  a  more  stimulating  environment,  and  under  less 
stringent  direction,  the  treatment  in  its  general  princi- 
ples can  be  continued. 

The  success  of  the  change  depends  mainly  on  the  skill 
with  which  the  program  is  arranged,  and  on  the  tact  with 
which  it  is  fulfilled.  Most  programs  seem  to  the  patient 
to  consist  mainly  of  commandments  to  do  nothing  desir- 
able. Hence  they  fail.  To  make  what  is  helpful,  pleas- 
ant and  what  is  pleasant,  helpful,  should  be  the  constant 
endeavor  of  both  physician  and  nurse.  Sometimes,  fret- 
ting due  to  inadequate  causes,  baseless  prejudice  against 
the  nurse,  and  intolerance  of  the  regime,  arise  to  detract 
from  the  benefit  of  the  change.  Those  of  us  who  have 
learned  little  else  from  Freud  and  his  disciples  have  at 
least  learnt  the  aid  which  just  such  complaints  may  be 
to  successful  treatment.  Instead  of  listening  with  our 
former  sufferance,  the  reaction  of  business  instinct  and 
courtesy  with  boredom,  we  are  now  alert  to  grasp  any 


TREATMENT  OF  MENTAL  STATE          211 

clue  to  the  patient's  condition  which  may  be  revealed  in 
his  murmurings ;  and  to  persist  in,  or  to  change,  details 
of  treatment  in  a  rational  manner.  The  more  direct  the 
medical  supervision  the  better  can  the  regime  be  adapted 
and  controlled.  Hence,  the  tabetic  should  remain  within 
reach  of  the  physician. 

Gradually,  as  isolation  and  discipline  are  now  lessened, 
effort  is  increased,  until  the  patient,  having  accumulated 
the  necessary  reserve  of  strength,  and  having  gained  in 
mental  capacity,  becomes  fit  to  return  to  his  former  en- 
vironment. Here  the  physician  encounters  usually  his 
greatest  difficulty — the  adjustment  of  the  tabetic's  daily 
effort  to  his  capacity.  Obviously,  to  confront  the  patient 
again  with  the  conditions  which  previously  defeated  him 
is  to  invite  another  disaster.  But  to  suggest  to  a  tabetic, 
not  conscious  of  important  physical  deterioration,  that 
he  should  give  up  his  employment,  alarms  him  and 
shakes  his  confidence.  The  adjustment  must  be  made, 
but  gradually,  tactfully.  So-called  efficiency  experts  or 
system  engineers  may  be  an  invaluable  aid  to  redistribut- 
ing the  work  of  a  business  so  as  to  relieve  a  tabetic  pro- 
prietor of  all  the  effort  not  needed  for  essential  direction. 
An  important  business  man  may  employ  a  secretary, 
allocate  his  routine  work  to  his  subordinates,  start  the 
day  later,  lengthen  the  midday  recess,  end  earlier,  and 
frequently  use  outdoor  exercise,  such  as  golf,  as  an 
excuse  for  a  day's  change.  The  commercial  traveler,  a 
frequent  tabetic,  may  stop  traveling  and  get  an  indoor 
post ;  the  telephone  inspector  may  change  from  outdoor 
to  office  duty ;  the  naval  commander  may  leave  an  arduous 
position  on  shore  for  a  peaceful  mission  on  the  high 
seas;  the  laborer  may  labor  mildly  on  piece  work  or 
become  a  janitor. 


212  LOCOMOTOK  ATAXIA 

Whatever  change  is  made  should  be  timely  and  should 
be  introduced  as  a  strictly  temporary  measure.  If  the 
change  be  adequate,  if  no  further  signs  develop,  greater 
activity  may  gradually  be  resumed.  Fluctuations  occur ; 
their  importance  must  not  be  overestimated ;  the  average 
condition  as  regards  sleep,  fatiguability  and  weight  from 
week  to  week  is  the  chief  guide  to  the  success  of  the  re- 
trenchment of  effort. 

The  initial  effect  of  reorganizing  the  daily  effort  may 
not  be  reassuring.  The  tabetic  may  fret  and  may  have 
difficulty  in  restricting  his  endeavors  to  their  new  scope. 
If  the  effort  demanded  in  the  new  task  is  not  too  great, 
this  stage  of  dissatisfaction  will  soon  pass.  But  the 
change  may  be  really  unsuitable.  Thus  my  naval  com- 
mander's peaceful  trip  was  unexpectedly  ended  by  the 
menace  of  war  and  he  had  to  resign;  the  inspector  find- 
ing office  routine  much  more  arduous  than  previous 
experience  had  led  him  to  expect,  took  up  other  work: 
one  has  now  been  a  preataxic  tabetic  for  seven  years,  the 
other  for  six  years. 

In  addition  to  restricting  effort,  the  tabetic  must  use 
the  rest  exercises  assiduously.  He  is  particularly 
exhorted  to  rest  after  any  strenuous  or  exciting  occur- 
rence. When  the  stress  of  circumstances  in  daily  life 
causes  nervous  tension,  he  must  not  permit  it  to  endure. 
Together  with  the  shortening  of  periods  of  high  tension 
and  the  maintenance  of  a  lower  average  level,  these  ex- 
ercises, systematically  practiced,  cause  oscillations  in 
.tension  to  be  less  easily  induced,  less  frequent,  and  of 
smaller  extent.  The  tabetic  should  also  continue  to  prac- 
tice his  exercises  in  movements  of  regular  rate,  gradu- 
ated duration  and  accurate  extent.  These  movements 
should  be  performed  with  the  utmost  attention  to  every 


TREATMENT  OF  MENTAL  STATE          213 

detail,  in  order  to  regulate  and  strengthen  his  control 
over  psychic  processes  and  to  prevent  the  usurpation  of 
cerebral  power  by  unnecessary  and  tyrannical  symptoms, 
such  as  ataxia. 


CHAPTER  XII 

PSYCHOTHERAPY  OF  PREATAXIC  SYMPTOMS 

Preataxic  symptoms.  Diplopia.  Pain,  measurement  and  analysis. 
Treatment  of  subacute  pain;  of  pain  crises.  Gastric  crises, 
measurement,  prevention.  Treatment  of  gastric  crises.  Cocain. 
Morphin.  Root  section.  General  principles  of  treating  pain,  gas- 
tric, and  other  crises.  Involuntary  micturition;  prevention,  treat- 
ment. Intestinal  and  genital  symptoms.  Blindness.  Deafness. 

REDUCING  the  expenditure  of  mental  energy  below  the 
income,  and  training  cerebral  action  so  that  achievement 
may  be  commensurate  with  effort  are,  we  have  seen,  the 
essential  principles  upon  which  we  base  the  treatment 
of  the  syphilitic  neurasthenic,  the  potential  paretic,  the 
potential  tabetic.  During  the  incipient  stage  of  tabes, 
the  neuralgic,  or  preataxic  stage,  the  only  stage  which 
should  ever  be  seen  in  tabes,  these  principles  are  rigor- 
ously applied.  As  the  tabetic  symptom  and  the  mental 
state  are  reciprocally  related,  this  treatment  of  the  men- 
tal state  prevents  or  minimizes  the  tabetic  symptoms. 

Unfortunately,  we  seldom  have  the  opportunity  to 
prevent  symptoms.  Patients  seek  our  aid  only  when 
symptoms  compel  recourse  to  us.  Then,  to  give  relief 
from  the  obnoxious  symptom,  we  treat  the  symptom 
mainly  through  the  mental  state  or  the  mental  state 
mainly  through  the  symptom,  according  to  the  nature  of 
the  symptom  (p.  185).  The  treatment  of  mental  state 
and  symptom  are  complementary. 

Before  beginning  the  treatment  of  any  symptom,  we 
must,  if  possible,  measure  it.  Measurement  is  the  only 

214 


PREATAXIC  SYMPTOMS  215 

means  by  which  we  can  accurately  estimate  the  results 
of  treatment. 

After  measuring  the  symptom  as  precisely  as  possible, 
we  endeavor  from  a  study  of  the  extent  of  the  lesions 
and  of  the  mental  state,  to  determine  the  importance  of 
the  structural  and  of  the  mental  changes  in  the  produc- 
tion of  the  symptom.  The  less  the  lesions  are  incrimi- 
nated, the  more  the  mental  state  is  blamable,  and  the 
more  rapidly  and  successfully  will  the  symptom  yield  to 
treatment. 

During  the  preataxic  period,  the  symptoms  for  which 
relief  are  sought  are  "nervousness,"  weakness  and 
fatigue,  diplopia,  pain,  crises,  bladder  trouble,  blindness 
and  deafness. 

The  treatment  already  outlined  will  quickly  relieve 
nervousness  and  fatigue. 

Diplopia  may  be  investigated  and  measured  by  the 
methods  previously  described  (p.  107).  It  usually  spon- 
taneously disappears.  It  seldom  persists  more  than  a 
few  days  after  exercises  in  eye  movements  (p.  206)  are 
begun.  By  such  movements  squint  may  often  be  re- 
moved, even  when  of  long  duration. 

The  benefits  conferred  by  oculists  through  treatment 
of  refraction  errors  emphasize  the  importance  of  dip- 
lopia and  of  visual  troubles  as  causal  factors  in  the 
mental  state  of  the  tabetic.  Patients  dislike  to  wear 
a  patch  over  the  misleading  eye.  I  insist  on  the  patch 
only  when  conscious  diplopia  is  present.  Attempts  to 
remove  the  need  for  unconscious  suppression  of  the 
false  image  by  correlating  the  eye  movements  are  usually 
partially,  but  are  seldom  completely,  successful. 

Few  symptoms  have  a  larger  mental  element  than  has 
pain.  By  pain  the  tabetic  accounts  to  himself  for  his 


216  LOCOMOTOR  ATAXIA 

feeling  of  incapacity;  by  pain  he  excuses  his  lack  of 
effort.  It  is  at  once  his  plea,  his  sentence  and  his  pardon. 
One  of  my  tabetics,  who  for  twelve  years  conserved 
his  pain  without  detriment  to  his  physique,  habitually 
slept  undisturbed  through  the  night;  awoke  painlessly 
towards  7  A.  M. ;  arose  and  began  to  dress.  At  this  stage 
in  his  daily  routine  he  was  seized  with  pain,  which  he 
expressed  by  crying  and  by  gyrating  about  his  bedroom. 
Pain  and  this  mental  state  were  practically  his  only 
symptoms.  The  hour  of  its  onset  suggests  that  the 
pain  was  provoked  by  a  more  or  less  unconscious  dread 
of  facing  the  day's  work.  When  I  first  saw  him  he  had 
maintained  this  curious  matutinal  reaction  for  years, 
during  which  his  able  and  devoted  wife  had  successfully 
assumed  the  burden  of  earning  for  both. 

One  suffers  lightly  a  pain  which  another  finds  words' 
inadequate  to  describe.  A  chronic  pain  which  the  tabetic 
bewails,  which  permits  sleep  of  ordinary  duration,  and 
which  is  unaccompanied  by  loss  of  weight,  has  not  the 
importance  which  the  tabetic  gives  it.  The  same  lesions 
that  produce  obsessing  anguish  in  one  may  cause  in 
another  only  an  insignificant  ache.  The  immensity  of  the 
pain  in  the  first  is  as  real  as  its  triviality  in  the  second. 
The  respiratory  movements  afford  a  most  delicate  index 
to  mental  processes.  We  can  roughly  measure  and 
record  the  mental  reaction  to  pain  by  applying  stimuli 
to  the  tabetic  while  his  respiratory  curve  is  being  graphi- 
cally recorded. 

Subjective  pain  in  the  tabetic  is  thus  of  two  kinds; 
one,  mainly  structural  in  origin,  intermittent,  transient, 
and  tending  spontaneously  to  cease.  The  other  pain 
probably  once  had  a  structural  basis  but  it  now  persists 
chiefly  as  a  phenomenon  of  the  tabetic's  mental  state. 


PEEATAXIC  SYMPTOMS  217 

This  latter  pain,  with  its  pseudo-crises,  waxes  and  wanes. 
It  is  greater  in  unfavorable,  less  in  favorable,  mental 
states.  Its  place  tends  later  to  be  usurped  by  ataxia  which 
affords  the  tabetic  a  more  adequate  expression  of  his 
mental  reactions.  Hence,  when  ataxia  develops,  pain 
often  decreases.  This  type  is  very  amenable  to  psycho- 
therapy. 

I  never  inquire  about  pain  unless  the  tabetic  reports 
it.  If  it  be  troublesome  he  will  surely  complain.  The 
testing  of  the  mental  reaction  to  pain  by  the  effect  upon 
respiration  of  pinpricks  and  other  slightly  painful  stim- 
uli; and  consideration  of  the  patient's  weight,  sleeping 
and  working  capacity,  together  with  his  mental  state,  en- 
able the  physician  to  form  a  fairly  just  opinion  of  the 
nature  and  real  importance  of  this  symptom.  Lack  of 
appreciation  of  the  true  basis  of  the  pain  state  leads  to 
futile  alcohol  injections  and  to  posterior  root  sections  in 
tabetics  who  would  suffer  pain  if  they  possessed  not  a 
single  surviving  pain  fiber. 

Pain  is  an  ideal  symptom  to  treat  by  indirection,  to 
treat  through  the  mental  state.  The  avoidance  of  all 
circumstances  unfavorable  to  mental  action,  the  insuring 
of  rest  and  the  regulation  of  the  mental  processes  alle- 
viate, and  often  banish,  it.  Pain  must  not  be  allowed  to 
interfere  with  treatment.  No  matter  how  much  com- 
plaint be  made,  the  rest  and  movement  exercises  should 
be  attempted.  If  the  effort  be  too  great  for  the  patient, 
his  pulse  will  increase  in  rate,  his  respiration  will  become 
jerky  and  other  objective  signs  of  failure  will  be  evident. 
Usually  after  a  few  minutes'  exercising,  complaints 
cease,  and  the  end  of  the  session  finds  the  patient  com- 
pletely relieved.  The  exercises  are  the  most  logical  and 
effective  method  of  treatment  we  possess  for  pain.  As 


218  LOCOMOTOR  ATAXIA 

the  mental  state  improves,  pains  diminish  in  frequency 
and  severity,  till  the  tabetic  ceases  to  mention  them. 

I  seldom  use  analgesics  for  subacute  pain.  The  rest 
exercises  and  local  heat  usually  enable  the  patient  to 
command  relief.  Occasionally,  high  frequency  has  been 
useful  to  reinforce  other  mental  influences.  Adequate 
bracing  of  the  foot  seems  also  to  exert  a  benign  influence 
on  pain. 

Crises  of  pain  are  mercifully  transient  and  tend  spon- 
taneously to  disappear.  In  crises,  every  palliative  ex- 
cept alcohol  and  opium  and  the  latter 's  derivatives  may 
be  tried.  Phenazonum,  five  grains,  acetanilid,  three 
grains,  and  caffein,  two  grains,  constitute  the  powder  I 
use.  In  very  severe  cases,  an  injection  of  ^  gr.  of  hy- 
oscin  hydrobromid  may  be  serviceable. 

There  are  cases  reported  of  pain  enduring  thirty  years 
and  being  the  unique  source  of  complaint  in  a  tabetic. 
We  are  grateful  if  we  can  so  far  protect  the  tabetic  that 
pain,  which  does  not  materially  diminish  his  capacity, 
is  the  sole  manifestation  of  his  disease.  Such  pain  is 
an  emotional  outlet  and  is  invaluable  to  him  as  a  warning 
and  a  curb  when  he  attempts  to  transgress  the  limits  of 
safety  in  effort. 

Gastric  crises  are  much  more  satisfactory  to  treat  than 
pain.  We  can  see  a  gastric  crisis  and  from  the  amount, 
nature,  and  frequency  of  the  vomiting,  and  from  the 
patient's  weight,  we  can  estimate  its  severity.  But  as 
the  attacks  are  self-limiting,  as  they  do  not  recur  for 
months,  and  sometimes  even  for  years,  as  in  some  tabetics 
they  are  frequent,  in  others  rare,  and  in  others,  again, 
unknown,  we  cannot  at  present  with  certainty  decide  the 
efficacy  of  treatment.  But  if  we  study  the  cause  of  the 
vagal  explosion  which  constitutes  a  gastric  crisis  (p. 


PKEATAXIC  SYMPTOMS  219 

128),  and  treat  it  rationally,  we  may  share  with  the  ta- 
betic his  satisfaction  from  the  alleviation  which  occurs, 
even  if  we  cannot  substantiate  our  claim  to  the  credit. 

I  have  already  dealt  with  the  condition  of  vagotonia 
(p.  190)  which  manifests  itself  in  gastric  discomfort, 
hyperacidity,  nausea  and  vomiting ;  which  is  due  to  men- 
tal stress,  and  which  may  be  a  prelude  to  gastric  crises. 
The  palliative  treatment  of  these  incipient  crises  we  saw 
consisted  in  reducing  vagal  activity  by  atropin,  hyoscin, 
and  allied  drugs  which  paralyze  the  vagus.  To  insure 
speedy  action,  accurate  dosing  and  psychological  effect, 
and  also  to  avoid  possible  gastric  disturbance  from  in- 
gestion,  these  drugs  should  be  administered  by  subcuta- 
neous injection.  Their  power  may  be  usefully  reinforced 
through  stimulation  of  the  sympathetic  by  adrenalin 
administered  per  rectum.  The  minimizing  of  local  irri- 
tation by  careful  dieting  should  not  be  neglected. 

But  the  essential,  the  curative,  treatment  consists  in 
improving  that  mental  state  to  which  the  vagotonia  is 
attributable.  In  the  study  of  the  mental  state  which 
precedes  its  treatment,  special  attention  should  be 
directed  to  the  possible  existence  of  direct  incentives  to 
nausea,  of  complexes,  especially  fear  complexes,  which 
utilize  nausea  as  an  emotional  expression. 

During  the  attack,  rest  is  the  sovereign  aid.  This  rest 
must  be  mental;  the  patient  should  be  kept  isolated, 
quiet  and  reassured:  and  physical;  the  patient  should 
lie  flat  on  his  back  in  bed  without  pillows:  and  local; 
no  food  or  drink  or  drug  should  add  to  the  gastric  irri- 
tability. An  ice  bag  applied  to  the  epigastrium  is  some- 
times valuable. 

In  addition  to  these  measures,  innocuous  doses  of  local 
and  general  sedating  drugs  are  used.  The  local  drug 


220  LOCOMOTOR  ATAXIA 

most  lauded  is  cocain.  It  is  supposed  to  anesthetize 
the  gastric  mucous  membrane.  The  amounts  recom- 
mended must  be  without  appreciable  effect  upon  the 
large  area  involved.  Any  anesthesia  which  cocain  in- 
duces lasts  only  minutes.  The  subsequent  irritative 
reaction  to  it  is  prolonged.  Its  use  for  gastric  crises 
should  be  discountenanced. 

Of  general  drugs,  morphin  and  its  derivatives  are  most 
used.  The  speedy  and  complete  oblivion  to  his  troubles 
which  the  tabetic  derives  from  morphin  endears  this 
drug  to  him.  Morphin  weakens  him  mentally  and  physi- 
cally. When  once  used,  it  demands  repetition.  It  be- 
comes a  reward  for  crises.  It  brings  local  and  general 
infections  in  its  train.  There  is  no  more  lethal  agent 
to  the  tabetic  than  morphin. 

Gastric  crises  seldom  last  more  than  forty-eight  hours. 
Easily  assimilated  food,  at  first  fluid,  later  mixed,  then 
solid;  at  first,  in  small  measured  quantities,  later  in 
larger ;  at  first,  at  infrequent,  later  at  frequent  intervals, 
soon  restores  to  the  tabetic  any  weight  he  may  have  lost. 

I  have  luckily  never  encountered  a  case  in  which  life 
was  menaced  by  gastric  crises.  But  by  those  who  have, 
heroic  treatment  has  been  advocated.  Forster  recom- 
mended the  cutting  of  certain  posterior  roots,  to  sever 
some  of  the  sensory  fibers  which  proceed  from  the  stom- 
ach to  the  central  nervous  system.  If  such  root  section 
can  prevent  gastric  crises,  then  an  intraspinal  injection 
of  novocain  at  the  level  of  these  roots  should  be  able 
abruptly  to  terminate  the  crisis.  I  am  not  aware  of 
any  satisfactory  demonstration  of  this  power.  I  tried 
it  twice  without  enough  success  to  tempt  me  to  try  it 
again.  I  have  no  personal  experience  of  Forster 's  opera- 
tion. The  only  case  in  which  it  was  practiced,  within  my 


PREATAXIC  SYMPTOMS  221 

immediate  circle,  died.  Of  twenty-five  resections  of  the 
seventh  to  the  ninth  or  tenth  posterior  thoracic  roots,  for 
gastric  crises,  reported  by  Forster  to  the  London  Royal 
Society  of  Medicine,  in  1911,  three  resulted  in  death,  two 
failed,  and  twenty  were  called  successful.  In  only  thir- 
teen of  these  twenty  was  there  no  return  of  the  crises; 
only  two  of  these  thirteen  had  been  observed  for  eighteen 
months.  There  is,  therefore,  a  mortality  in  the  hands  of 
the  protagonist  of  this  treatment  of  twelve  per  cent. 
For  this  mortality,  the  maximum  success  demonstrated 
is  relief  from  crises  for  eighteen  months  in  two  out  of 
twenty-five  cases,  i.e.,  in  eight  per  cent.  Such  success 
is  dearly  bought.  Ere  now  there  have  probably  occurred 
more  deaths  from  this  operation  alone  than  are  at- 
tributed to  gastric  crises  in  all  medical  literature  since 
tabes  was  first  recognized.  The  failure  of  the  operation 
has  only  led  Forster  to  recommend  the  extension  of  the 
operative  field,  and  Exner  to  advise  the  section  of  the 
tenth,  eleventh  and  twelfth  roots. 

Root  section  has  also  been  tried  for  the  relief  of  light- 
ning pains;  but  it  has  fortunately  been  abandoned. 

When  a  pain,  a  bladder,  a  rectal,  a  gastric,  a  laryngeal 
or  other  crisis  appears,  it  should  be  palliated;  when  it 
passes,  its  effects  should  be  repaired;  provocation  of  a 
recurrence  should  be  avoided;  and  the  mental  state 
should  be  zealously  treated.  The  success  of  psycho- 
therapy and  the  infrequency  with  which  pain  or  gastric 
or  other  crises  interrupt  the  placidity  of  the  blind,  show 
that  alleviating  the  mental  state  is,  at  present,  the  best 
means  at  our  disposal  for  treating  these  symptoms. 

Excepting  diplopia,  involuntary  micturition  is  the 
easiest  of  the  tabetic  symptoms  to  cure.  Involuntary 
micturition,  as  I  have  pointed  out  (p.  134),  is  due  to  the 


222  LOCOMOTOR  ATAXIA 

tabetic's  habit  of  infrequently  and  imperfectly  emptying 
his  bladder.  It  is  a  symptom  which  should  never  occur. 
Every  tabetic  should  be  warned  that  he  must  urinate 
at  definite  hours  irrespective  of  his  need.  If  a  tabetic 
under  medical  treatment  develops  dribbling,  it  implies 
either  his  disobedience  or  the  physician's  neglect. 

In  bladder  disturbance  complicated  by  cystitis,  the 
bladder  should  be  mechanically  emptied  at  regular  and 
frequent  intervals  and  should  be  flushed  by  bland  warm 
saline  solutions  till  the  returning  fluid  is  clear.  For  this 
purpose  only  a  sterile  soft  rubber  catheter  is  permissible. 

Usually  all  that  is  needed  is  urination  at  prescribed 
hours.  In  urinating,  the  incontinent  tabetic  should 
assume  the  attitude  which  is  mechanically  most  favorable 
for  emptying  the  bladder,  the  position  in  which  the  intra- 
abdominal  pressure  is  highest,  the  crouching,  squatting 
attitude,  a  low  sitting  attitude  in  which  the  thighs  are 
well  flexed  on  the  abdomen. 

The  aid  of  the  sound  of  running  water  may  be  helpful. 
Urination  should  be  attempted  for  five  minutes  every  two 
hours.  No  fluid  should  be  taken  for  two  hours  before 
retiring;  and  at  first,  the  bladder  may  then  need  to  be 
emptied  by  catheter. 

This  regular  emptying,  without  waiting  for  sensory 
demands,  prevents  accumulation  of  urine  in  the  bladder, 
and  maintains  the  bulk  of  the  bladder  contents  below  the 
containing  capacity.  Dribbling  is  therefore  avoided  and 
with  it  the  distressing  soiling  of  the  tabetic's  garments. 
The  bladder  wall  is  no  longer  unduly  distended.  The 
stretched  blood  vessels  relax  and  dilate.  The  blood  sup- 
ply increases  and  the  bladder  muscle  and  sphincter  regain 
their  tone.  With  increase  of  tone,  the  containing  power 
of  the  bladder  and  the  expelling  force  grow. 


PREATAXIC  SYMPTOMS  223 

During  urination  the  patient  should  practice  breathing 
and  relaxation  exercises  and  should  attend  to  the  sensa- 
tions which  accompany  the  urinary  act.  This  attentioii 
enables  him  to  perceive  the  feeble,  imperfect  sensory 
images  which  he  has  been  ignoring ;  and  soon  he  acquires 
dependence  upon  them. 

The  urinary  intervals  should  gradually  be  lengthened, 
the  attitude  should  progressively  approach  that  nor- 
mally employed.  Usually  only  two  or  three  weeks'  prac- 
tice is  needed  to  reestablish  a  useful  degree  of  control. 

Analogous  measures  relieve  difficulty  in  defecation.  I 
have  already  mentioned  the  return  of  virility  which 
patients  whose  mental  state  is  being  successfully  treated 
not  uncommonly  report. 

In  tabetic  optic  atrophy,  the  measurable  variation  of 
visual  acuity  which  accompanies  alteration  in  the  mental 
state  seems  to  promise  that  psychotherapy  will  benignly 
influence  blindness.  But  I  have  never  succeeded  in  pro- 
ducing in  tabetics  who  are  becoming  blind  a  mental  state 
which  was  stable  and  permanently  favorable  to  vision. 
The  impending  darkness  daunts  them  beyond  reassur- 
ance. Nor  have  I,  in  the  few  cases  in  which  I  have  tried, 
been  able  to  arrest  the  progress  by  complete  visual  rest 
and  by  psychotherapy.  In  two  cases  who  were  rapidly 
losing  their  sight,  as  a  last  resort,  I  used  mescalin  (p.  88), 
hoping  I  might  restore  their  confidence  and  conserve 
some  of  the  drug's  action,  by  demonstrating  to  them  that 
they  possessed  a  visual  power  so  far  exceeding  what 
they  daily  used.  In  neither  did  the  increased  acuity 
survive  the  action  of  the  drug.  The  only  cases  in  which 
I  have  been  able  to  benefit  vision  to  a  measurable  extent 
by  psychotherapy  are  those  in  whom  merely  perception 
of  light  remained.  If  the  syphilitic  invasion  finally  halts 


224  LOCOMOTOR  ATAXIA 

before  this  stage  is  reached,  analogous  improvement 
should  be  procurable;  but  I  have  no  experience  of  it. 
Treatment  of  the  mental  state  of  the  blind  tabetic  renders 
his  blindness  less  intolerable.  The  measures  I  have  out- 
lined are  for  the  blind  tabetic  merely  a  prelude  to  useful 
occupational  exercises. 

The  auditory  capacity  in  the  seemingly  deaf  is  often 
astounding.  Unsuspected  by  the  physician  even  a  suffi- 
cient number  of  cochlear  fibers  may  persist  to  allow 
the  reestablishment  of  a  useful  degree  of  hearing. 

During  the  improvement  in  the  mental  state  which 
accompanies  rest  and  exercises,  hearing  spontaneously 
improves.  The  recovery  of  hearing  sometimes  takes  an 
unusual  course  which  further  emphasizes  its  psychic 
nature ;  thus,  one  of  my  tabetics,  deaf  as  the  proverbial 
post  in  ordinary  social  intercourse,  now  experiences  no 
difficulty  in  hearing  telephonic  communications.  Apart 
from  training  the  mental  state  and  teaching  the  impor- 
tance of  hearing  the  first  word — that  is,  of  immediately 
directing  all  attention  to  hearing — I  have  not  attempted 
to  treat  the  deaf  tabetic. 

In  a  paper  which  I  read  to  the  Otological  Section  of 
the  New  York  Academy  of  Medicine,  in  1914,  I  empha- 
sized the  psychic  factor  in  deafness  and  the  tendency 
of  deafness  to  increase  with  stationary  lesions.  I  pointed 
out  that  there  is  a  more  or  less  dominant  tone  in  every 
sound  by  which  we  distinguish  and  interpret  it ;  and  that 
in  the  same  sound  we  each  may  recognize  a  different  tone 
as  dominant.  I  suggested  that  those  trained  to  recognize 
a  sound  by  one  tone  may,  if  the  fibers  conducting  that 
tone  be  destroyed,  learn  to  recognize  it  by  some  other 
tone  subserved  by  fibers  which  have  escaped.  I,  there- 
fore, urged  that  every  deaf  tabetic  should  be  carefully 


PKEATAXIC  SYMPTOMS  225 

tested  by  means  of  the  Edelmann-Bezold,  or  a  kindred 
apparatus,  throughout  the  entire  range  of  the  human 
auditory  scale;  that  the  surviving  tones  should  be  care- 
fully charted;  that  training  in  the  perception  of  the 
surviving  tones,  at  first,  tone  by  tone,  in  varying  inten- 
sities, and  next  in  combination  should  then  be  practiced; 
and  that,  finally,  the  interpretation  of  sounds  by  means 
of  these  tones  should  be  taught.  Blindfolding  will  make 
this  training  easier  and  more  successful. 


CHAPTER  XIII 

TREATMENT  OF  MOTOR  SYMPTOMS  OF  TABES 

Faulty  equilibration  first  motor  disorder  in  tabes:  its  measurement, 
analysis,  and  prognosis.  Ataxia,  its  prevention  and  measurement. 
Minimizing  ataxia  by  reducing  movement  and  by  mechanical  sup- 
ports. Defects  of  the  tabetic  foot  as  a  support.  Means  of  ascer- 
taining and  of  remedying  these  defects.  New  method  of  obtaining 
cast  of  foot  in  action.  Foot  brace.  Special  tabetic  shoe.  Braces 
for  joints.  Value  of  belt  and  bandages.  Temporary  use  of  all 
appliances. 

ROMBERG'S  sign,  swaying  abnormally  when  standing 
with  closed  eyes,  is  the  first  indication  in  the  tabetic  of 
inadequate  mental  control  over  movement. 

The  amount  of  swaying  may  be  measured  by  the 
cephalograph  which  records  not  only  the  extent  but  also 
the  planes  of  the  swaying.  But  this  instrument  is  ines- 
sential. We  can  roughly  estimate  the  degree  to  which 
equilibration  is  disturbed  by  the  attitude  necessary  to 
make  its  disturbance  apparent ;  or  by  the  attitude  neces- 
sary to  insure  stability;  or  by  the  length  of  time  the 
highest  stable  attitude  can  be  maintained. 

In  addition  to  measuring  the  power  to  maintain  the 
attitude  of  the  body  as  a  whole,  we  measure  the  power 
to  maintain  the  position  of  every  limb,  and  of  every  sec- 
tion of  a  limb,  and  the  postural  sense  in  the  respective 
joints. 

The  primary  cause  of  the  deterioration  of  attitude,  the 
underlying  root  or  vestibular  lesions,  should  be  sought 
through  the  motor  and  sensory  signs  which  reveal  them. 
The  less  extensive  the  lesions  are,  the  greater  is  the 

226 


TREATMENT  OF  MOTOR  SYMPTOMS   227 

disparity  between  the  loss  of  postural  sense  in  the  distal 
and  in  the  proximal  joints ;  and  between  the  loss  of  pos- 
tural sense  and  the  loss  of  the  power  to  maintain  posture. 
With  this  disparity  will  be  found  evidence  of  mental 
fatigue,  of  lack  of  attention,  and  of  rapid  development 
of  the  instability — all  signs  of  a  dominant  mental  element 
in  the  symptom,  all  promises  that  speedy  and  gratifying 
improvement  will  follow  appropriate  mental  treatment. 

If  the  mental  treatment  of  the  pretabetic  be  timely  and 
adequate,  lack  of  equilibration  will  seldom  develop.  If 
lack  of  equilibration  be  promptly  and  wisely  treated, 
ataxia  will  not  occur,  except  as  the  direct  consequence 
of  some  sudden  calamity.  As  the  treatment  of  instability 
differs  in  no  essential  from  the  treatment  of  ataxia,  and 
as,  in  practice,  instability  and  ataxia  usually  together 
confront  us,  to  avoid  repetition,  we  shall  deal  with  the 
treatment  of  instability  as  it  arises  in  the  course  of 
ataxia. 

We  saw  (p.  77)  that  all  the  influences  which  conduce 
to  fear,  fatigue,  depression,  excitement,  anger  and  other 
mental  states  unfavorable  to  movement  constitute  so 
many  incentives  to  ataxia,  so  many  ataxic  complexes; 
and  that  the  liability  to  ataxia,  or  the  measure  of  ataxia, 
may  be  expressed  by  the  ratio : 

Ataxic  complexes. 
Coefficient  of  ataxia  =  — 

Coordinating  power. 

When  the  value  of  this  coefficient  equals  unity  the  thresh- 
old of  ataxia  is  almost  reached. 

In  treating  the  preataxic  tabetic,  our  aims  were  to 
reduce  his  effort  to  his  capacity;  to  remove  influences 
which  perpetuated  his  mental  stress ;  to  train  him  in  rest, 
to  enable  him  to  accumulate  a  reserve  of  mental  energy ; 


228 


LOCOMOTOR  ATAXIA 


and  finally  to  train  him  in  cerebral  control  so 
as  to  make  the  results  he  attained  commensu- 
rate with  his  efforts.  The  achievement  of 
these  aims  would  reduce  the  ataxic  complexes, 
the  numerator  of  this  ratio,  and  increase  the 
cerebral  control,  the  denominator ;  would  les- 
sen, therefore,  the  value  of  the  coefficient  of 
ataxia,  would  prevent  ataxia.  The  tabetic 
who  is  ataxic  is  merely  a  tabetic  whose  men- 
tal state  has  been  allowed  to  deteriorate  be- 
low the  level  necessary  for  effective  action,  a 
tabetic  whose  treatment  has  been  neglected. 

Before  treating  an  ataxic,  we  determine  by 
analysis  of  his  attitude  and  movement  the  es- 
sential factors  in  their  disorder  and  we  ob- 
tain a  record  of  the  ataxia. 

In  order  to  record  his  gait,  the  ataxic  dips 
his  feet,  clad  in  socks,  into  a  solution  of  po- 
tassium permanganate.  If  he  can  walk  only 
with  the  aid  of  a  stick,  the  end  of  his  stick  is 
covered  with  cotton  fixed  by  thread  and  also 
dipped  in  the  permanganate.  He  then  walks 
upon  a  strip  of  paper,  40  inches  wide.  This 
paper  is  that  used  for  the  printing  of  news- 
papers, and  is  supplied  in  a  large  roll.  Each 
patient  walks  about  fifteen  paces,  and,  as  he 
walks,  the  imprints  of  the  end  of  his  stick 
and  of  his  feet  are  left  upon  the  paper. 
This  imprinted  paper  is  then  cut  off, 
dated,  and  the  name  written  upon  it.  For 
purposes  of  reproduction,  it  is  photo- 
graphed on  a  greatly  reduced  scale  (see  Fig- 
ure 83).  Subsequent  sets  of  foot  impres- 


4 


r 


93 

i 

O 

JS 
o 


O 


o 

fe 


TREATMENT  OF  MOTOR  SYMPTOMS   229 

sions  graphically  record  the  progress  of  the  treatment. 

The  mental  state  is  woefully  deranged  by  the  onset 
of  this  inexplicable,  bewildering,  relentless  symptom, 
ataxia,  which  threatens  the  very  essence  of  activity, 
movement.  And  every  movement,  according  to  the  degree 
to  which  it  is  ataxic,  further  decomposes  the  mental 
state. 

The  more  an  ataxic  walks,  the  more  ataxic  he  becomes. 
It  is  difficult  to  cure  a  symptom  which  is  constantly  being 
aggravated.  No  mental  relief  is  so  great  as  that  'Which 
arises  from  the  relief  of  the  ataxia.  The  most  obvious 
relief  measure  is  reducing  movement — the  use  of  con- 
veyances, the  bringing  of  the  home  nearer  to  the  place 
of  work  or  business.  But  still  more  valuable  are  mechan- 
ical aids  to  stability.  Any  ataxic  who  can  walk  with  a 
stick  can  walk  without  a  stick.  Yet  the  stick  immediately 
reduces  the  effort  to  walk.  The  more  advanced  the  case, 
the  greater  is  the  benefit  which  mechanical  aid  confers. 
The  kind  and  the  amount  of  the  needed  aid  differ  in 
almost  every  case,  and  for  any  particular  case  can  be 
ascertained  only  by  careful  examination.  To  inflict  un- 
necessary appliances  is  as  unwise  as  to  deny  needed 
support.  I  shall  describe  the  ^mechanical  treatment  of 
a  case  of  ataxia  of  average  severity,  merely  as  an  in- 
dex of  the  mode  in  which  the  problem  should  be  con- 
fronted. 

When  standing,  the  average  ataxic  tabetic  rotates  his 
feet  outwards  in  a  horizontal  plane,  around  a  vertical 
axis,  which  passes  through  the  ankle  joint,  to  such  an 
extent  that  the  distance  between  the  great  toes  may  be 
several  times  that  which  separates  the  heels.  These 
abducted  feet  are  sometimes  overpronated,  and  in  such 
cases  both  the  anteroposterior  and  transverse  arches 


230 


LOCOMOTOR  ATAXIA 


usually  yield.  Such  a  foot  affords  a  wretchedly  inade- 
quate support.  The  only  stable  element  in  it  may  be 
the  os  calcis:  the  foot  may  move  as  a  flail  attached  to 
the  ankle:  in  front  of  the  os  calcis,  it  may  be  only 

a  flabby  conglomeration  of 
bones.  The  hypotonic 
muscles  of  such  a  foot  elon- 
gate. The  ligaments  stretch 
perhaps  beyond  functional 
utility.  I  have  seen  an  in- 
crease of  an  inch  in  length 
and  of  an  inch  in  breadth 
occur  when  the  body  weight 
was  placed  upon  the  foot. 
The  tabetic  with  these  ab- 
ducted, pronated,  formless 
feet,  in  his  necessity,  clings 
to  the  ground  with  his  toes. 
During  this  simian  action, 
which  is  partly  a  reflex  ex- 
pression of  fear,  the  mid- 
dle joints  of  the  toes  are 
arched  against  the  box  of 
the  shoe.  The  ataxic,  more- 
over, often  dorsiflexes  his 
foot  and  toes  as  a  prelude 
to  the  movement  of  flexion  at  the  hip  joint  in  walking 
Sometimes  the  abducted  feet  are  supinated,  the  patient 
walking  on  the  os  calcis  and  base  of  the  fifth  metatarsal. 
In  such  feet  the  clutching  with  the  toes  is  even  more 
marked  than  in  the  pronated  feet;  but  although  both 
arches  suffer,  the  displacement  of  the  tarsal  bones  is 
less  constant. 


FIG.  84. — Footprints  showing  the 
habitual  attitude  of  the  feet  in  the 
slightly  ataxic.  Note  the  distance 
between  the  heels  is  much  less 
than  that  between  the  big  toes. 


TREATMENT  OF  MOTOR  SYMPTOMS   231 


The  clutching  of  the  ground  with  the  toes  and  the 
excessive  dorsiflexion  of  the  foot  cause  blisters  and  cal- 
lous formation  on  the  tips  of  the  toes,  where  they  rub 
against  the  sole  of  the  shoe,  and  over  the  dorsal  aspect 
of  the  middle  joints,  especially  of  the  second  and  third 
toes,  which  come  in  contact  with 
the  box  of  the  shoe. 

The  lack  of  support  which  the 
feet  afford  to  the  swaying  tabetic 
creates  in  him  not  merely  uncer- 
tainty at  every  step,  but  even  a 
lively  fear.  The  instability  and 
fear  result  in  prodigal  expendi- 
ture of  muscular  and  nervous  en- 
ergy and  contribute  to  fatigue. 
Thus,  the  troubles  of  the  ambulant 
ataxic  multiply. 

When  the  feet  are  separated  so 
that  each  external  malleolus  is  in 
the  same  vertical  plane  as  the 
great  trochanter,  and  the  long  axis 
of  each  foot  is  directed  forward, 
making  the  feet  parallel  (see  Fig. 
94),  the  feet  are  in  the  position 
which  confers  the  greatest  amount 
of  stability  in  standing.  In  this 
position,  the  weight,  bearing  on 
each  foot,  is  distributed  across  the 

longitudinal  and  transverse  arches,  and  is  directly  trans- 
mitted to  the  ground  by  a  tripod,  consisting  first,  of  the 
internal  tubercle  of  the  os  calcis;  second,  of  the  sesa- 
moid  bones  and  the  head  of  the  first  metatarsal;  and 
third,  of  the  base  of  the  fifth  metatarsal. 


FIG.  85. — Shows  initial  state 
of  a  tabetic.  The  blur- 
ring of  the  picture  is 
due  to  his  unsteadiness. 
Note  the  broad  base, 
contorted  attitude,  and 
the  need  of  the  stick  in 
standing.  A  second 
photograph  (Fig.  94) 
was  taken  six  weeks 
later.  (Grossman.) 


232 


LOCOMOTOR  ATAXIA 


The  tabetic  foot  should  be  braced  in  such  a  manner 
that  in  this  proper  position  the  full  weight  will  be  borne 
on  the  natural  tripod  in  standing  and  in  walking.  In 
order  to  achieve  this  accurately,  in  addition  to  the  usual 

procedure  of  recognizing 
a  diminution  in  the  longi- 
tudinal arch,  and  correct- 
ing this  along  the  lines  in- 
dicated by  a  cast  of  the 
foot  taken  in  a  position  of 
rest,  we  need  to  obtain  a 
cast  of  the  foot  in  the  act 
of  bearing  the  full  weight 
of  the  body.  A  compari- 
son of  this  cast  with  that 
taken  of  the  foot  at  rest 
shows  exactly  the  points 
on  which  the  weight  is 
falling,  the  degree  to 
which  the  natural  arches 
have  given  way,  and  the 
amount  of  spread  in  all 
directions,  which  is  per- 
mitted by  the  overstretch- 
ing of  the  ligaments  and 
muscles 

FIG.  86. — Shows  broad  base,  crouching 

attitude  and  the  anxious  vigilance          To  obtain  the  Cast  of  the 
necessary  to  maintain  it.  f()ot    ^   ^.^    Dr     gora_ 

pure  and  I  proceed  as  follows :  Two  tin-plate  boxes,  four- 
teen inches  long  and  seven  inches  wide,  with  removable 
sides  two  inches  high,  are  half  filled  with  dental  wax, 
which  has  a  melting  point  of  110°  F.  The  boxes  accommo- 
date any  size  of  foot.  They  can  be  fixed  parallel  to  one 


;  all  possible  variations  in  the  longitudinal  arch 
s  no  standard  brace  for  the  tabetic  foot;  what 
>ther;  every  tabetic  foot  should  be  treated  as  a 

233 


234 


LOCOMOTOR  ATAXIA 


another  at  any  desired  distance,  by  means  of  rigid  con- 
necting rods.  The  Loxes  ire  placed  in  water,  which  is 
allowed  to  heat  to  about  116°  F.,  then  all  the  wax  thor- 
oughly softens.  The  softened  wax  is  carefully  kneaded, 
into  a  smooth  layer  of  uniform  thickness,  covering  com- 
pletely the  bottom  of 
the  box.  The  patient 
is  shown  how  to  stand 
with  the  feet  parallel, 
and  separated  by  a 
distance  equal  to  the 
width  at  the  hips. 
Then  he  practices 
placing  one  foot,  say, 
his  right,  squarely 
upon  the  .ground, 
"^P^  meanwhile  resting  his 
weight  upon  the  phy- 


FIG.  88. — Footprint  1  was  taken  when  the 
foot  was  bearing  no  weight;  2,  when  the 
foot  was  bearing  the  weight  of  the  body. 
Note  the  remarkable  spread  of  the  foot 
in  2;  its  length  and  breadth  are  both  in- 
creased. 


sician ;  next  placing 
his  left  upon  the 
ground,  parallel  with 
the  right;  and  then, 
supported  by  the 

physician  only  enough  to  prevent  swaying,  allowing  his 
weight  to  be  borne  wholly  upon  his  feet.  After  two  or 
three  trials,  this  maneuver  is  easily  accomplished.  The 
two  boxes  are  lifted  out  of  the  hot  water,  braced  together 
at  the  desired  distance,  and  placed  in  front  of  the  patient. 
The  patient,  leaning  upon  the  physician,  places  first  his 
right  foot  squarely  upon  the  wax  in  the  right  box,  next  his 
left  foot  squarely  upon  the  wax  in  the  left  box,  and  then 
allows  all  his  weight  to  rest  upon  his  feet;  while  doing 


TREATMENT  OF  MOTOR  SYMPTOMS   235 

so,  he  is  supported  by  the  physician  sufficiently  to  prevent 
swaying.  In  about  two  minutes,  the  temperature  of  the 
wax  in  the  box  falls  below  the  melting  point,  the  wax 
solidifies,  and  the  patient,  once  more  leaning  his  whole 
weight  upon  the  physician,  then  removes  his  feet  from 
the  boxes.  In  each  box,  there  now  remains,  deeply  im- 
pressed in  the  solid  wax,  the  imprint  of  the  patient's 
foot  as  it  was  when  his  weight  was  fully  upon  it.  Into 


la  2a 

FIG.   89. — Footprint  la  was  taken  when  the  foot  was  bearing  no  weight. 
Footprint  2a  shows  the  same  foot  bearing  the  weight  of  the  body. 


this  mold,  fluid  plaster  of  Paris  is  poured  and  allowed  to 
set.  Then  by  placing  the  boxes  again  in  water  above 
110°  F.,  the  wax  softens,  and  the  plaster  casts  can  be 
lifted  out. 

If  the  temperature  of  the  water  be  allowed  to  rise  too 
high,  and  then  to  cool  too  suddenly,  the  wax  becomes 
hard  and  brittle.  It  can  be  restored  to  its  original  plastic 
state  by  being  again  heated,  and  very  slowly  allowed  to 
cool.  The  only  precautions  necessary  in  choosing  the 
wax  are,  first,  that  the  w^ax  be  solid  at  body  temperature ; 
and,  second,  that  its  melting  point  be  within  a  few  degrees 


236  LOCOMOTOR  ATAXIA 

of  the  body  temperature,  so  that  the  patient  may  not  step 
into  wax  which  is  uncomfortably  hot. 

Plaster  casts  are  now  taken  of  the  foot  at  rest,  in  the 
usual  way — the  leg  crossed  upon  the  opposite  knee  and 
supported  in  the  position  of  least  constraint,  while  the 
cast  is  being  taken. 

We  are  now  provided  with  a  plaster  cast  of  the  foot 
in  action  and  a  plaster  cast  of  the  foot  at  rest.  With 
these  two  casts  as  guides,  we  build  a  third.  In  building 
this  third  cast,  our  effort  is  to  utilize  the  normal  pressure 
points  in  the  foot  and  to  restore,  as  far  as  we  can,  the 
normal  bony  arrangement  of  the  foot,  the  pressure 
tripod.  For  this  purpose  we  use  the  cast  of  the  foot  at 
rest ;  add  plaster  to  it  at  points  where  we  wish  to  avoid 
pressure,  and  scrape  away  plaster  at  points  where  we 
wish  to  allow  pressure.  This  modified  cast  is  the  model 
of  the  foot  upon  which  the  brace  maker  fashions  the 
plate. 

The  cast  of  the  foot  in  action  shows  usually  that  the 
faulty  position  assumed  throws  the  weight  on  the  pos- 
terior and  outer  limb  of  the  tripod.  Sometimes,  all  the 
weight  is  borne  on  the  heel;  sometimes,  on  the  heel  and 
the  internal  limb  of  the  tripod;  and  sometimes  on  the 
heel  and  outer  limb  of  the  tripod.  In  a  condition  such 
as  the  last,  the  weight  falling  on  the  os  calcis  and  the 
base  of  the  fifth  metatarsal  and  the  foot  supinated — the 
following  are  the  main  points  which  guide  us  in  con- 
structing the  model  for  the  brace  maker.  The  posterior 
part  of  the  longitudinal  arch,  between  the  tubercle  of 
the  os  calcis  and  the  base  of  the  fifth  metatarsal,  is 
increased  sufficiently  to  throw  the  foot  inwards,  and  by 
diminishing  the  convexity  of  the  heel  across  the  tubercle 
of  the  os  calcis,  the  foot  is  thrown  forward,  both  planes 


TREATMENT  OF  MOTOR  SYMPTOMS   237 

converging  on  the  inner  limb  of  the  tripod,  until  the 
weight  falls  squarely  on  each.  Our  aim  is  to  pronate  the 
foot,  without  pressing  on  the  inner  side  more  than  is 
needed  to  guide  the  supinated  foot  into  the  proper  degree 
of  pronation.  The  model  is  made  more  wide  than  the 
cast  of  rest,  but  narrower  than  the  cast  of  action,  so  as 
to  limit  the  spread  and  yet  not  compress  the  tissues 
unduly.  The  lengthening  of  the  foot  is,  of  course,  dim- 
inished by  the  longitudinal  arch  support.  The  spread  of 
the  transverse  arch  is  also  diminished  by  increasing  the 
concavity  between  the  two  anterior  limbs  of  the  tripod, 
and  by  extending  the  brace  completely  across  the  space. 

The  brace  is  a  modification  of  the  Whitman  brace. 
The  inner  lip  is  curved  below  the  level  of  the  scaphoid; 
the  outer  flange  is  the  lower  and  does  not  extend  so  far 
forward ;  and  the  support  of  the  transverse  arch  extends 
outwards  beneath  the  four  inner  toes.  When  the  spread 
is  very  great,  the  inner  lip  is  extended  forward  to  include 
the  first  metatarsophalangeal  joint,  surrounding  it  com- 
pletely on  the  inner  side. 

No  two  pairs  are  exactly  alike,  each  being  built  on  its 
own  model,  constructed  from  the  casts  of  the  foot  at 
rest  and  in  action. 

The  brace  is  light,  accurately  applied,  and  efficient. 
It  supports  the  foot  in  action.  This  support  is  obtained 
as  the  result  of  study  of  the  foot  in  action,  which  has 
shown  us  the  distribution  of  the  pressure  upon  the  foot. 
Braced  by  this  plate,  the  foot  is  no  longer  a  treacherous, 
structureless  prop,  but  sustains  pressure  on  the  normal 
pressure  points,  and  affords  reliable  support  from  every 
part  of  its  surface. 

This  braced  foot  is  encased  in  a  high  shoe  or  boot, 


238 


LOCOMOTOE  ATAXIA 


devised  by  us  and  made  by  Mr.  Max  Deutsch  of  New 
York. 

A  straight  last  is  used.  The  sole  projects  three-eighths 
of  an  inch  around  the  upper.  A  hickory  wood  filler  ex- 
tends from  the  heel,  through  the  shank,  to  the  front  of 
the  sole,  rendering  the  sole  rigid  and  unbending.  The 
heel,  wedge-shaped,  with  the  base  of  the  wedge  on  the 


FIG.  90. — The  tabetic's  boot.    Diagrams  to  show  how  rigidity,  lightness,  and 
support  are  attained  in  its  construction. 

ground,  is  seven-eighths  of  an  inch  high,  has  its  inner  and 
outermost  layers  of  leather,  and  the  two  intermediate 
layers  of  cork,  enveloped  in  leather.  A  special  feature 
is  made  of  the  snugness  of  the  fit  in  the  longitudinal 
arch.  The  box  of  the  shoe  is  high.  The  upper  is  made  of 
calf.  Around  the  ankle,  between  the  lining  and  the  upper, 
is  a  small  reinforcing  leather  brace.  A  thick,  soft  tongue 
enables  the  shoe  to  be  tightly  laced.  The  total  weight  of 
a  shoe  (size  8,  on  an  A  last)  is  just  less  than  fourteen 
ounces. 

The  special  features  of  this  shoe  are,  first,  its  rigidity, 


TREATMENT  OF  MOTOR  SYMPTOMS   239 

from  the  moment  the  foot  is  put  flatly  upon  the  ground, 
all  movement  ceases;  there  is  no  more  oscillation;  the 
foot  has  an  unbending  support:  second,  its  lightness 
which  permits  the  tabetic  to  walk  more  with  less  fatigue ; 
third,  the  increased  ground  area  of  the  heel  and  of  the 
sole,  which  augments  the  foothold ;  and  fourth,  the  ankle 
support  which  prevents  the  ankle  from  yielding.  A 
patient,  thus  shod  and  braced,  can  use  his  whole  foot, 


FIG.  91. — The  tabetic's  boot.  Note  that  the  boot  rests  securely  on  the 
ground;  its  ground  surface  is  quite  level  and  has  a  larger  area  than  an 
ordinary  shoe. 

instead  of  his  heel,  as  a  support.  The  foot  in  front  of 
the  os  calcis,  instead  of  being  an  unstable,  is  now  a 
rigid,  support.  In  feet  so  braced,  local  and  remote  pains 
diminish,  and  disappear.  Shooting  pains  in  the  legs 
seem  to  decrease  both  in  severity  and  in  frequency.  Ap- 
parently these  pains  can  be,  to  a  certain  extent,  reflexly 
initiated  by  local  irritation  in  the  foot,  and  the  removal 
of  that  local  irritation  diminishes  them.  Blisters  and 
callous  formation  disappear.  The  patient  now  does  not 
oscillate  every  time  the  foot  is  put  down.  He  walks  on 
a  secure,  rigid  base.  He  is  more  stable.  He  feels  more 
stable.  He  fears  less;  and  as  fear  begets  ataxia,  and 
ataxia  begets  fear,  his  increased  reassurance  greatly  im- 


240 


LOCOMOTOR  ATAXIA 


proves  his  gait.     The  patient  thus  supported  is  soon 
weaned    from    the    straddle-legged    attitude    which    in 

tabetics  renders  coordinate  walk- 
ing so  difficult. 

This  method  of  treating  the 
foot  is  essentially  temporary.  By 
means  of  exercises  we  increase 
the  tone  of  the  hypotonic  muscles 
until  the  muscles  themselves  are 
capable  of  maintaining  the  bones 
in  the  correct  position.  In  me- 
chanically supporting  the  foot 
we  aim  solely  to  maintain  the  foot 
in  a  correct  position,  and  to  sup- 
port it  there,  until  such  time  as 
the  muscular  support  may  be  suf- 
ficiently developed  to  fulfill  this 
function  unaided. 

In  addition  to  supporting  the 
feet  it  may  be  necessary  to  but- 
tress the  knees  and  the  back  un- 
til the  skeleton  can  acquire  its 
best  support,  the  support  of 
strengthened  muscles.  Over- 
stretched muscles  can  neither  re- 
inforce joints  nor  increase  in 
tone.  Abnormal  mobility  of  the 
joints  must,  therefore,  be  pre- 
vented. But  the  prevention  must 
not  immobilize:  movement  is 
essential  to  muscular  health. 
Nor  must  the  restricting  apparatus  be  heavy  or 
irksome.  Rarely  a  light  corset  is  needed.  More  often 


FIG.  92. — Showing  band- 
ages used  as  temporary 
muscles. — "For  cases  in 
which  abduction  and 
outward  rotation  of  the 
lower  limbs  are  present, 
the  bandage  is  tied  to 
the  loop  on  the  back  of 
the  boot  by  which  the 
boot  is  pulled  on;  then 
it  is  carried  to  the  outer 
side  of  the  leg  and  wound 
spirally  round  the  leg. 
The  free  end  is  ... 
fixed  to  a  belt  .  .  /" 
Bandages  should  not  be 
applied  next  to  the  skin. 


TREATMENT  OF  MOTOR  SYMPTOMS   241 


a  simple  belt;  sometimes,  only  a  bandage.  The  value 
of  the  bandage  as  a  temporary  artificial  muscle  is  its 
adaptability;  its  drawback,  the  task  of  reapplying  it 
daily.  The  mode  of  application  depends  on  the  case. 
For  cases  in  which  abduction  and  outward  rotation  of  the 
lower  limbs  are  present  the  bandage  is  tied  to  the  loop 
on  the  back  of  the  boot  by  which  the  boot  is  pulled  on ; 
then  it  is  carried  to  the  outer  side  of  the  leg  and  wound 

spirally  round  the  leg.  Two 
spiral  turns,  one  of  which 
passes  behind  the  knee,  usu- 
ally suffice.  The  free  end  is 
passed  once  around  the  waist 


FIG.    93.— Showing 

used  as  temporary  muscles. 
Bracing  of  a  tabetic  whose 
back  is  weak  and  whose 
knees  give.  Bandages 
should  not  be  applied  next  • 
to  the  skin. 


FIG.  94. — Same  patient 
as  in  Fig.  85.  To  show 
effect  of  treatment. 
(Grossman.) 


.and  tied  or  fixed  to  itself,  to  a  belt  or  to  a  corset.    Both 
legs  may  need  this  treatment  (Fig.  92). 


242 


LOCOMOTOR  ATAXIA 


The  shoulders  may  be  braced  back  by  a  double  spica 
or  a  St.  Andrew's  Cross  bandage,  from  which  connect- 
ing bands  pass  to  the  corset,  or  belt,  or  to  the  bandage 
fixed  round  the  waist.  (Figs.  92  and  93.) 

By  such  simple  means 
ataxies  reeling  on  two 
sticks  may  be  at  once  in- 
duced to  walk  freely  with- 
out their  sticks  in  private, 
and  to  rely  on  one  stick  in 
public.  The  mental  effect 
of  this  bracing  is  good. 
The  bracing  corrects  the 
attitude  which  is  perpet- 
uating the  fear,  and  fa- 
tigue of  the  mental  state. 
It  stabilizes  the  ataxic. 
It  abruptly  ends  the  de- 
pression* which  his  pro- 
gressing incapacity  en- 
gendered. It  enables  ac- 
tivity to  be  carried  on  with 
reduced  effort.  It  permits 
movement  in  attitudes 
which  have  not  yet  been 
learnt.  It  accelerates  and 
facilitates  treatment. 

Such  devices  are  purely 
temporary.  The  braces  must  be  gradually  loosened,  and, 
one  by  one,  discarded  as  the  muscular  tone  improves  and 
as  equilibrium  and  coordinate  movement  are  reacquired. 
They  must  be  carefully,  not  indiscriminately,  used.  Eco: 
nomic  conditions  sometimes  force  the  tabetic  to  continue 


FIG.  95. — Same  patient  as  in  Fig.  86. 
To  show  effect  of  treatment.  (Gross- 
man.) 


TREATMENT  OF  MOTOR  SYMPTOMS   243 

more  active  than  he  should.  Mechanical  aids  are  then 
indispensable  in  minimizing  his  enforced  efforts,  but  they 
must  not  be  permitted  to  lull  the  ataxic  into  neglect  of 
the  systematic  treatment  of  his  mental  state,  the  only 
treatment  which  can  control  his  disability  and  can  render 
him  really  effective. 


CHAPTER  XIV 

TREATMENT    OF    DISORDERS    OF    MOVEMENT    IN    TABE,S 

(CONTINUED) 

Removal  of  muscular  constraint.  Easy,  confident,  and  perfect  move- 
ment founded  upon  appreciation  of  postural  images.  Measures 
to  insure  appreciation  of  postural  images.  Blindfolding.  Train- 
ing in  attention  and  in  capacity  for  effort.  The  maintenance  of 
optimal  conditions  throughout  the  treatment.  Training  in  attitude 
recumbent,  sitting,  "all  fours,"  kneeling,  standing.  Dosage  of 
postural  exercises.  Training  in  movement  in  these  several  atti- 
tudes as  they  become  stabilized.  The  cardinal  qualities  of  simple 
movements.  Simple  movements.  Complex  movements.  Stabiliz- 
ing the  base  for  progression.  Progressing.  Creeping.  Kneeling. 
Walking.  Dosage  of  movement  exercises.  Walking  in  public. 

AFTER  analyzing  and  measuring  the  disorder  of  move- 
ment, and  after  adopting  such  measures  as  prevent  the 
further  aggravation  of  that  disorder,  we  proceed  to  cure 
it.  As  disorder  of  movement  arises  mainly  from  deterio- 
ration of  the  mental  state  below  the  level  necessary  for 
effective  action,  its  treatment  should  comprise  avoidance 
of  the  conditions  which  produced  the  mental  deteriora- 
tion, rest,  training  in  attention,  and  the  systematic  order- 
ing of  the  mental  processes.  Mental  exercises  which 
afford  an  externalized  result  by  which  the  mental  process 
may  be  judged,  controlled  and  perfected,  are  essential 
to  the  ordering  of  the  mental  processes.  Improvement 
in  the  mental  state  by  these  measures  is  accompanied  by 
diminution  of  the  ataxia.  The  improvement  in  move- 
ment is  a  measure  of  the  improvement  of  the  mental 
state;  and  that  improvement  should  be  such  that  the 
tabetic  regains  the  preataxic  state. 

244 


DISORDERS  OF  MOVEMENT  245 

Movement  and  attitude  are  muscular  externalizations 
of  mental  processes.  Accurately  to  reflect  a  mental  proc- 
ess in  muscular  action  requires  a  musculature  free  from 
all  constraint. 

There  should  be  no  obscuring  of  the  desired,  by  an 
existing,  muscular  expression.  The  less  the  admixture  of 
muscular  expressions,  the  more  perfectly  the  movement 
mirrors  the  desire.  Before  evoking  a  new  muscular 
expression  we  should  remove  all  that  is  obliterable  of  the 
old.  Perfect  movement  cannot  be  impressed  upon  the 
hidebound  tabetic.  Before  the  teaching  of  movement  is 
attempted,  the  ataxic,  through  the  rest  exercises,  must  be 
freed  from  all  the  contortions  and  rigidities  which  former 
mental  states  and  exigencies  of  movement  have  imprinted 
upon  his  musculature. 

The  blind,  directed  mainly  by  their  postural,  pressure 
and  tactile  senses,  move  coordinately.  Normal  individ- 
uals, in  habitual  movements,  such  as  walking,  are  simi- 
larly but  unconsciously  directed  (p.  75).  When  the  feeble, 
delayed  and  imperfect  peripheral  after-images  of  move- 
ment mislead  the  tabetic,  he  ignores  and  suppresses  them. 
He  criticizes,  guides  and  corrects  every  movement  by  aid 
of  vision.  During  movement  his  attention  is  more  or  less 
wholly  devoted  to  overseeing  his  movements.  He  be- 
comes a  visual  automaton.  When  he  moves,  he  thinks 
only  of  moving.  Unless  he  carefully  scrutinizes  his 
movements,  he  cannot  move. 

A  watched  normal  movement  is  clumsy:  a  watched 
tabetic  movement  is  ataxic  and  involves  effort  which 
brings  fatigue.  The  increasing  vigilance  which  move- 
ment demands  is  a  constant  strain  on  the  tabetic :  he  may 
not  move  without  care  and  foresight;  he  dreads  every- 
thing he  does  not  see.  Moving  by  vision  is  moving  with 


246  LOCOMOTOE  ATAXIA 

dread  and  effort.  Such  movement  is  clumsy  and  destruc- 
tive of  the  tabetic's  mental  capacity.  The  tabetic  must 
be  taught  to  move  easily,  confidently,  freely  and  unaided 
under  all  circumstances.  He  must,  therefore,  be  taught 
to  move,  not  in  response  to  his  visual,  but  to  his  postural, 
images.  The  postural  images  which  he  habitually 
despises  and  suppresses,  he  must  learn  to  discern,  to  ap- 
preciate and  to  utilize.  He  must  attend  to  his  postural 
images. 

To 'insure  attention  to  these  feeble,  delayed,  imperfect, 
postural  images,  external  distraction  must  be  obviated 
by  decreasing  competition  for  attention  between  postural 
images  and  images  of  other  sensory  fields:  a  mental 
state  must  be  procured  which  is  as  free  as  possible  from 
internal  distraction,  from  fear,  excitement  and  other  emo- 
tional influences  detrimental  to  attention,  detrimental 
to  the  perception  of  postural  images :  and  fatigue  must 
be  avoided,  for  the  greater  the  fatigue,  the  less  is  the 
power  to  attend  to  the  postural  images. 

In  early  life,  the  impulses  that  underlie  sensations  of 
pressure  preempt  attention.  Pressure  soon  falls  from 
this  eminence  as  touch  and  taste  associations  become 
more  numerous.  These,  however,  grow  progressively 
less  important  in  their  turn  for  they  soon  are  relatively 
few  compared  with  the  myriad  of  associations  from  the 
visual  field.  As  experiences  accumulate,  the  visual  asso- 
ciations far  outnumber  the  associations  from  all  the 
other  sensory  fields.  A  visual  stimulus,  therefore,  evokes 
an  image  that  excites  incomparably  more  associations 
than  a  tactile,  an  auditory,  or  a  postural  image.  Effort- 
less attention  in  the  normal  adult  is  largely  mortgaged 
to  vision. 

In  the  darkness  and  silence  of  the  night  an  insignificant 


DISORDERS  OF  MOVEMENT  247 

discomfort  of  the  day  may  become  an  obsessing  pain. 
Tea-tasters  and  wine  connoisseurs,  when  they  wish  to 
appreciate  a  flavor,  close  their  eyes  as  they  smell  and 
taste.  Everyone  has  noticed  the  fixed  stare,  the  rapt 
gaze,  of  the  unsophisticated  being  made  to  marvel. 

To  obviate  external  distraction,  to  enable  attention  to 
be  focussed  upon  postural  images,  irrespective  alike  of 
the  extent  of  their  demand  and  of  the  number  of  memory 
images  of  posture  which  the  tabetic  possesses,  the  tabetic 
must  minimize  the  competition  of  his  visual  images  for 
attention.  Absence  of  visual  images  from  the  competi- 
tion for  attention,  focusses  attention  upon  postural 
images  and  confers  upon  the  blind  a  perception  of  pos- 
ture one-fourth  more  sensitive  than  the  seeing  possess 
(p.  59). 

Ataxic  tabetics  who  have  become  blind  may  recover 
their  lost  power  to  .perceive  posture  and  become  less 
ataxic.  Indeed,  we  have  seen  that  they  may  lose  sponta- 
neously every  trace  of  incoordination.  The  feeble,  im- 
perfect, and  delayed  postural  images  which  result  from 
the  tabetic  lesion  contain  adequate  guidance  not  merely 
for  the  blind  tabetic's  movements  but  may  suffice  even  to 
direct  the  movement  of  his  ataxic  colleagues  (Abraham- 
son's  case,  p.  99). 

To  minimize  external  distraction  and  to  focus  attention 
upon  postural  images,  we  teach  the  ataxic  to  move  blind- 
folded. To  blindfold,  we  use  a  mask1  made  of  soft  wash- 
able cloth,  which  is  fixed  to  the  head  by  means  of  tapes. 
Every  ataxic  should  have  two  masks,  for  his  exclusive 
use.  The  blindfolded  ataxic  is  an  attentive,  a  quick,  and 
a  successful  pupil. 

1  Masks  and  knee  guards  are  obtainable  from  Kny-Scheerer  Com- 
pany, New  York  City. 


248  LOCOMOTOR  ATAXIA 

To  procure  freedom  from  internal  distraction  and  to 
avoid  fatigue,  we  use  the  rest  exercises  (p.  196).  Unless 
his  mental  state  be  tranquil,  the  tabetic  can  learn  little ; 
unless  he  has  a  reserve  of  strength,  his  pulse  leaps  even 
at  the  thought  of  movement ;  and  without  the  initial  train- 
ing in  attention  which  these  exercises  confer  he  is  momen- 
tarily a  prey  to  fresh  distractions. 

By  blindfolding,  distraction  is  avoided  and  attention 
is  concentrated.  By  the  rest  exercises,  a  musculature 
as  free  as  possible  from  unconscious'  muscular  contrac- 
tions, and  a  composed,  placid  and  attentive  mental  state 
are  obtained.  Both  mentally  and  physically,  the  tran- 
quil, blindfolded  ataxic  is  in  the  most  favorable  state  for 
training  in  normal  movement. 

Throughout  the  training,  these  optimal  conditions  must 
be  maintained.  There  must  be  the  most  careful  gradua- 
tion of  the  amount  of  effort  demanded  from  the  ataxic, 
and  when  his  capacity  for  effort  is  reached,  rest  and 
recuperation  must  follow.  The  effort  required  from  him 
varies  with  the  difficulty  and  the  duration  of  the  exer- 
cises. The  easiest  must  be  the  initial  exercises  and  their 
amount  must  be  well  within  his  fatigue  limit.  To  con- 
trol an  ataxic  movement  is  more  difficult  than  to  perform 
the  most  complex  normal  movement.  So  the  initial  train- 
ing in  cerebral  control  is  gained  with  respiratory  move- 
ments, with  eye  movements,  with  movements  of  non- 
ataxic  limbs. 

No  successful  movement  is  possible  unless  the  relation 
of  the  body  to  its  environment  is  stable ;  unless  there  is 
a  fixed  point  to  move  upon;  unless  equilibrium  can  be 
maintained  during  the  movement.  Movements  should 
be  grafted  only  upon  correct  well  balanced  attitudes. 

The  recumbent,  the  posture  in  which  the  equilibrium 


DISOEDEES  OF  MOVEMENT  249 

of  the  body  is  mechanically  and  passively  assured,  is 
occasionally  the  only  posture  which  the  ataxic  can  at 
first  maintain;  but  almost  invariably  sitting  can  be 
achieved. 

In  the  sitting  posture  he  can  gain  valuable  training 
in  stability  for  the  erect  attitude.  He  may  at  first  need 
an  arm  chair  to  support  the  head  and  trunk:  later,  he 
can  sit  erect  on  a  stool  without  back  or  arms.  Next,  he 
practices  with  one,  then  with  both  arms  outstretched  at 
the  level  of  the  shoulders  or  held  above  his  head.  Finally, 
in  his  outstretched  hands  he  supports  weights.  Similar 
exercises  are  later  practiced  in  the  kneeling  and  in  the 
standing  postures. 

After  the  sitting  posture,  "all-fours"  is  learnt.  On 
all  fours,  the  head  should  be  held  well  up,  the  body 
straight,  the  thighs  at  right  angles  to  the  trunk,  the 
Jlower  limbs  parallel,  the  feet  slightly  dorsiflexed,  and 
the  toes  on  the  ground.  The  feet  at  first  may  need  the 
bracing  effect  of  a  friendly  wall  and  the  posture  may 
require  aid  for  its  maintenance.  Such  aid  should  be  un- 
sparingly given  and  only  withdrawn  as  improvement 
warrants.  In  the  all-fours  attitude,  the  amount  of  aid 
required  is  usually  very  slight  and  is  soon  dispensed 
with. 

After  stability  on  all-fours  is  gained,  kneeling  is  prac- 
ticed. Besides  swaying,  the  tendency  here  is  to  bend 
forward  from  the  hips.  Great  care  should  be  used  to 
procure  a  proper  upright  attitude,  with  the  head  and 
trunk  erect.  After  acquiring  first  sitting,  next  all-fours, 
and  then  kneeling,  the  tabetic  finally  learns  to  stand. 
Stability  in  the  erect  posture  depends  largely  upon  the 
thoroughness  of  the  preliminary  training  of  the  head  and 
trunk  and  lower  limbs  in  the  sitting,  all-fours,  and  kneel- 


250  LOCOMOTOR  ATAXIA 

ing  postures,  and  upon  the  adequacy  of  the  mechanical 
bracing  of  the  foot  and  lower  limbs. 

The  length  of  time  for  which  a  posture  is  maintained 
should  be  carefully  measured.  At  first  the  tabetic  may 
be  able  to  preserve  his  posture  only  for  a  few  seconds. 
Succor  should  always  be  immediate  and  effective  so  that 
no  cause  for  unnecessary  fear  shall  complicate  the  task. 
When  the  patient  is  placed  in  a  posture  a  warning  "Get 
ready,"  followed  after  an  agreed  interval  by  "Now," 
marks  the  withdrawal  of  aid.  Then  counting  is  com- 
menced, the  patient  having  been  told  to  maintain  his 
posture  for  a  definite  time.  With  repetition  this  time 
is  gradually  lengthened. 

The  dosage  of  the  postural  exercises,  their  difficulty, 
frequency  and  duration,  should  be  scrupulously  regu- 
lated; should  always  remain  well  within  the  fatigue 
limit;  and  should  only  be  increased  with  the  raising  of 
that  limit.  Every  posture  should  be  learnt  blindfolded 
and  should  be  practiced  till  it  becomes  effortless. 

Contemporaneously  with  the  postural  exercises,  move- 
ment should  be  taught.  As  no  movement  is  permissible 
except  in  a  correct,  well  balanced  posture,  and  as  the 
recumbent  may  be  the  only  perfect  posture,  the  move- 
ment exercises  must  often  be  first  practiced  recumbent. 
As  more  difficult  attitudes  are  stabilized,  movement  is 
commenced  in  them.  Thus,  while  the  erect  sitting  atti- 
tude is  being  learnt,  movements  in  the  recumbent  posture 
are  practiced ;  while  the  all-fours  attitude  is  being  learnt, 
movements  in  the  sitting  attitude  are  practiced ;  while  the 
erect  standing  position  is  being  learnt,  movements  in  the 
other,  easier,  and  already  acquired  attitudes  are  prac- 
ticed. 

The  simplest  movements  are  the  least  disordered  and 


DISORDERS  OF  MOVEMENT  251 

they  are  the  easiest  to  perfect.  They  are,  therefore, 
taught  first.  The  perfection  of  a  simple  movement  de- 
pends upon  the  perfection  of  its  cardinal  qualities, 
strength,  direction,  extent  and  rhythm. 

For  training  in  strength,  resistance  exercises  are  em- 
ployed. These  resistance  exercises  begin  before  move- 
ment is  taught.  The  patient's  head  or  trunk,  thigh, 
knee  or  foot  is  placed  in  an  attitude  which  he  is  exhorted 
to  maintain  for  a  given  period,  against  the  physician's 
efforts  to  move  it.  The  period  should  at  first  be  short, 
two  or  three  seconds,  and  should  be  gradually  increased 
to  ten  seconds.  The  timing  must  be  audible.  These 
exercises  are  varied  by  the  patient's  attempting  to  move 
against  the  physician's  immobilizing  resistance.  The 
resistance  exercises  are  a  great  aid  to  postural  sense  ap- 
preciation. 

Most  of  the  weakness  of  tabes  is  mental,  not  muscular. 
Even  when  it  is  muscular,  graduated,  passive  and  active 
resisted  movement  is  its  best  cure.  But  massage  and 
electricity  may  usefully  aid.  Massage  at  first  should  be 
light  and  should  be  applied  only  to  a  part  of  the  body, 
for  say,  five  to  ten  minutes ;  later,  it  should  progressively 
increase  in  strength,  and  should  gradually  extend  to  com- 
prise the  whole  body.  Electricity  may  aid  the  tone  of 
the  muscles.  Its  physical  consequences  may  be  insignifi- 
cant, although  its  mental  effect  is  conspicuous.  It  should 
be  mild  and  painless.  With  galvanism,  large  electrodes 
must  be  used  to  avoid  burning.  Mild  electrical  treat- 
ment lends  a  useful  informality  to  psychotherapeutic  en- 
quiry. I  seldom  use  either  massage  or  electricity. 

The  beginning  and  the  end  of  every  movement  should 
be  definitely  fixed.  The  series  of  postural  images  which, 
comprise  the  movement  should  be  invariable.  The  more 


252  LOCOMOTOR  ATAXIA 

often  the  same  images  are  linked  the  readier  and  the 
more  inevitably  do  they  associate  with  one  another  and 
not  with  postural  images  unrelated  to  the  series,  and 
the  more  rapid  and  perfect  becomes  the  movement.  Fre- 
quent repetition  engraves  these  images  and  their  se- 
quence upon  the  tabetic's  memory. 

Instruction  in  the  direction  and  extent  of  a  movement 
begins  by  the  physician's  passively  performing  the  move- 
ment upon  the  blindfolded  tabetic.  Then  the  tabetic 
resists  the  passive  movement.  Next  the  tabetic's  at- 
tempts to  perform  the  movement  are  guided.  The  guid- 
ance is  gradually  diminished  as  the  movements  gain  in 
accuracy.  The  difficulty  of  a  simple  movement  varies 
with  its  range.  The  initial  movements  should  be  of 
small  extent. 

For  training  in  rhythm  and  rate,  vocal  timing  is  excel- 
lent. A  loud  ticking  watch  or  clock  is  useful.  But  best 
is  the  ordinary  metronome,  'obtainable  at  all  music  deal- 
ers. Every  ataxic  should  have  one  for  his  private  use. 
All  movements  should  at  first  be  performed  slowly,  but 
not  too  slowly.  The  initial  optimal  rate  can  readily  be 
ascertained  by  trial.  This  rate  must  gradually  quicken, 
but  not  at  the  expense  of  efficient  action. 

A  movement  is  not  perfect  till  it  can  be  well  performed 
at  all  speeds,  against  resistance.  After  an  interval  which 
varies  with  the  individual,  and  which  is  longer  the  more 
complex  the  movement,  the  movement  is  so  acquired  that 
the  eliciting  of  the  desired,  in  association  with  the  exist- 
ing, postural  images,  excites  in  order  the  images  which 
link  them,  and  the  movement  is  performed  with  a  mini- 
mum of  effort. 

In  our  appreciation  of  the  body's  posture,  the  domi- 
nant images  from  the  head  and  trunk  are  more  important 


DISORDERS  OF  MOVEMENT  253 

than  those  from  the  limbs;  those  from  the  legs,  than 
those  from  the  arms;  and  those  from  large,  than  those 
from  small  joints.  Most  rapid  progress  is  attained  when 
these  various  sections  are  trained  in  the  order  of  their 
importance. 

To  teach  the  recumbent  patient  to  move,  we  first  relax 
him.  After  general  relaxation  has  been  practiced,  atten- 
tion is  specially  focussed  on  the  head. 

The  recumbent  ataxic  with  the  muscles  of  his  head 
and  neck  relaxed,  the  shoulders  supported  on  a  sandbag 
and  the  head  extended,  is  instructed  to  count  slowly  while 
the  physician  at  a  uniform  rate  repeatedly  moves  the 
head  to  a  position  of  flexion,  pauses,  and  then  returns  it 
to  the  original  extended  position.  Next,  the  patient 
lightly  but  steadily  resists  the  passive  movement.  Then, 
the  movement  is  practiced  with  the  patient  performing 
and  the  physician  aiding  and  guiding.  The  physician's 
aid  gradually  lessens  as  improvement  occurs,  until  the 
movement  is  executed  by  the  patient  alone.  Finally  the 
movement  is  made  against  resistance.  A  movement 
which  caimot  be  made  against  resistance  is  still  faulty. 

Every  movement  is  timed  first  by  the  physician,  then 
by  the  patient,  finally  by  the  metronome.  Movements  at 
first  are  slow :  as  they  are  perfected  they  are  quickened ; 
finally,  practice  is  obtained  in  varying  the  rate  with  that 
of  the  metronome.  This  training  in  time  is  essential  to 
smooth,  easy  movement. 

The  trunk  is  similarly  exercised.  In  the  recumbent 
posture,  while  exercising  the  trunk,  at  first,  the  tabetic 
has  his  feet  fixed,  a  rope  in  his  hand,  and  the  teacher's 
aid.  Gradually  these  auxiliaries  are  eliminated. 

The  training  of  head  and  of  trunk  may  be  varied  by 


254  LOCOMOTOR  ATAXIA 

changing  from  the  recumbent  to  the  sitting  and  from 
the  sitting  to  the  recumbent  posture. 

Besides  head  and  trunk,  limb  movements  may  be  prac- 
ticed in  the  recumbent  attitude. 

After  general  relaxation,  attention  is  directed  espe- 
cially to  relaxing  one  limb,  say  the  right  lower.  Relaxa- 
tion of  the  hip,  knee  and  ankle  are  then  in  turn  procured. 
The  hip  is  first  dealt  with,  next  the  knee,  then  the  hip  and 
knee,  then  the  ankle,  and  finally  hip  and  knee  and  ankle 
together,  so  that  the  degree  of  muscular  relaxation  in  the 
chosen  limb  shall  be  as  great  as  is  obtainable. 

The  postural  sense  loss  in  the  hip  is  less  than  that  in 
the  knee,  in  the  knee  than  in  the  ankle,  in  the  ankle  than 
in  the  toes.  The  greater  the  number  of  surviving  pos- 
tural impressions  in  any  joint,  the  greater  is  the  ease 
with  which  movement  at  that  joint  can  be  made  coordi- 
nate. Training  in  movement  should  start  at  the  hip, 
then  proceed  to  the  knee  and  finally  to  the  ankle. 

At  first,  all  teaching  should  be  confined  to  flexion  and 
extension.  The  legs  may  be  supported  at  right  angles  to 
the  thighs,  on  a  chair  or  board,  while  active  unaided 
flexion  and  extension  of  the  thigh  on  the  abdomen  is 
practiced.  A  light  posterior  splint  may  usefully  im- 
mobilize the  knee  when  first  flexion  and  extension  of  the 
lower  limb  are  taught.  Lateral  and  rotatory  movements 
may  need  to  be  controlled  by  bandages.  These  mechan- 
ical aids  are  soon  discarded. 

After  the  hip,  the  knee  movements  are  practiced. 
There  the  patient's  task  is  simple,  for  only  flexion  and 
extension  are  possible.  Also,  as  less  strength  is  needed, 
the  tabetic  does  not  tire  so  quickly  from  knee  as  from 
hip  movements.  The  knee  movements  are  practiced  by 
allowing  the  leg  to  hang  over  the  end  of  the  couch;  the 


DISORDERS  OF  MOVEMENT  255 

recumbent  tabetic  exercises  first  on  his  back  and  later 
face  downwards. 

After  the  hip,  the  knee,  and  then  the  ankle,  first  of 
the  same  limb  then  of  its  fellow,  are  educated  in  flexion 
and  extension.  In  every  exercise,  first  relaxation,  next 
passive,  next  again  passive  resisted,  then  active  guided, 
later  active  unaided,  and  finally  active  resisted  move- 
ments are  practiced.  When  the  hip  movements  are  ac- 
quired, then  the  movement  exercises  begin  with  hip 
movements :  when  knee  movements  are  perfected,  the 
lesson  begins  with  hip,  then  proceeds  to  knee  and  last 
to  the  yet  unlearned  ankle  movements.  The  repetition 
of  a  movement  which  can  be  well  performed  is  a  good 
introduction  to  the  learning  of  the  yet  imperfect  move- 
ment. 

The  movements  acquired  in  the  recumbent  are  prac- 
ticed in  the  sitting,  in  the  all-fours,  in  the  kneeling,'  and 
in  the  standing  attitude,  as  these  attitudes  are  succes- 
sively stabilized. 

Complex  movements,  such  as  creeping  and  walking, 
are  compounded  of  simple  movements.  When  the  direc- 
tion and  extent  of  the  component  simple  movements  have 
been  acquired,  these  movements  should  be  practiced  in 
sequence  so  that  the  series  of  postural  images  which 
belong  to  each  of  the  several  components  may  be  linked 
together.  Then  the  eliciting  of  any  one  series  elicits  the 
images  of  the  allied  series  in  order.  The  tabetic  acquires 
functional  facilitation  among  his  postural  images. 

In  the  recumbent  and  in  the  sitting  posture,  the  move- 
ments of  the  limbs  necessary  for  creeping  and  walking 
should  be  practiced.  If  such  movements  cannot  be  per- 
formed when  the  patient  is  spared  the  effort  to  balance, 


256  LOCOMOTOR  ATAXIA 

much  less  can  they  be  performed  when,  in  addition  to 
the  movements,  the  patient  must  also  balance. 

Progression  demands  the  power  to  maintain  posture 
not  merely  in  the  usual  stationary  attitudes  but  also 
on  the  diminished  base  of  support  which  is  inherent  to 
progression.  Stability  upon  this  diminished  base  is  a 
necessary  preliminary  to  progression.  Progression  is 
acquired  first  in  the  most  stable  posture  for  progressing, 
the  creeping  posture,  a  posture  which  involves  active 
movements  only  at  the  hip  and  shoulder;  then  in  the 
kneeling;  and  finally  in  the  standing.  The  first  steps 
should  be  small  and  slow.  To  insure  direction  in  blind- 
fold progression,  I  use  strips  of  carpet  or  of  linoleum. 
For  novices,  strips  three  to  four  feet  wide  are  necessary. 
The  width  decreases  as  the  movements  improve. 

The  knees  in  creeping  should  be  protected.  I  use  knee- 
guards  somewhat  similar  to  those  used  by  carpenters. 
These  knee-guards  consist  of  two  rolls  about  nine  inches 
long  and  one  inch  in  transverse  section,  made  of  stout 
cloth  stuffed  with  hair,  which  are  fixed  parallel,  at  a 
distance  of  about  one  and  a  half  inches,  upon  a  layer 
of  thick  carpet.  Above  this  carpet  layer,  between  the 
parallel  rolls,  the  patient's  knee  rests,  and  thus  is  pre- 
vented from  touching  the  ground.  This  knee-guard  gives 
good  protection.  It  also  gives  considerable  support  for 
it  broadens  the  kneeling  surface  and  prevents  the  patient 
from  rolling.  A  soft  continuation  extends  from  the 
guard  about  two  inches  upwards.  To  this  continuation 
and  to  the  guard,  tapes  are  sewn.  Every  pair  of  tapes 
has  a  buckle  by  which  it  is  fixed  around  the  limb.  The 
tapes  keep  the  guard  in  place  (Fig.  96). 

Shoes  must  be  worn  while  creeping,  in  order  to  protect 
the  toes. 


DISORDERS  OF  MOVEMENT 


257 


In  creeping,  a  step  involves  the  temporary  loss  of  one 
of  the  four  supports ;  hence,  creeping  is  possible  only  if 
the  patient  can  balance  for  the  duration  of  that  step  on 
the  remaining  tripod.  The  patient  first  learns  to  throw 
his  weight  in  turn  on  the  four  possible  tripods,  the  left 
hand,  left  knee,  right  knee;  right  hand,  left  knee  and 
right  knee;  left  hand,  right  hand,  left  knee;  left  hand, 
right  hand,  right  knee. 
Lifting  first  a  hand,  and 
later  a  knee,  from  the  floor 
is  then  practiced  till  sta- 
bility can  be  maintained 
on  any  of  the  four  tripods. 
When  stability  on  all- 
fours  is  gained,  and  stabil- 
ity on  three  points,  then 
one  hand  is  moved  for- 
ward, the  weight  redis- 
tributed, and  then  the 

hand  is  moved  back.  The  soles  of  the  feet  should  rest 
against  a  wall;  from  the  wall,  the  foot  moves  forward 
when  the  thigh  is  flexed  and  the  knee  is  lifted  off  the 
ground;  to  the  wall  the  foot  is  returned,  on  completing 
the  movement.  After  exercising  one  side,  the  other  side 
is  exercised.  Later  the  maneuver  may  be  reversed ;  first 
the  hand  is  moved  backwards,  and  then  the  knee. 

Creeping  is  first  performed,  moving  limb  by  limb  at 
command.  Thus,  at  the  word  "One,"  the  right  hand 
is  moved  forward;  at  "Two,"  the  right  knee;  at 
"Three,"  the  left  hand;  at  "Four,"  the  left  knee.  The 
usual  tendency  is  for  a  small  step  to  be  made  by  the 
hand  and  a  large  one  by  the  knee;  both  hand  and  knee 
must  move  forward  equal  distances.  The  knees  in  move- 


FIG.  96. — "The  knees  in  creeping 
must  be  protected. "  Any  efficient 
knee  guards  may  be  used.  Those 
shown  here  are  satisfactory. 


258  LOCOMOTOR  ATAXIA 

ment  tend  to  be  abducted  and  circumducted ;  they  must 
be  moved  straight  forward.  The  feet  fly  from  the 
ground,  and  also  separate  widely.  They  must  be  kept 
parallel  and  the  toes  must  remain  on  the  ground.  It  is 
sometimes  easier  to  begin  with  backward  creeping. 

When  proficiency  in  creeping  is  gained,  then  kneeling 
is  practiced.  Next,  the  weight  is  balanced  first  on  one 
knee,  then  on  the  other.  Then  one  knee  after  the  other 
is  momentarily  raised ;  and  then  small  forward  steps  are 
made.  At  first  the  tabetic  merely  shuffles  the  knees 
slowly  along  the  ground ;  later  he  moves  more  freely  and 
quickly;  but  always  he  remains  erect. 

Finally  walking  is  taught.  The  blindfolded  patient, 
standing  facing  and  near  to  a  wall,  for  reassurance  and 
possible  support,  throws  his  weight  from  one  foot  to  the 
other  by  command  for  a  measured  length  of  time.  This 
he  practices  till  he  can  change  his  balance  from  foot  to 
foot  as  fast  as  the  metronome  can  beat.  Next  he  prac- 
tices rising  on  the  toes  of  one  foot,  then  of  the  other 
and  then  on  the  toes  of  both  feet  simultaneously.  Now, 
not  changing  his  place,  he  lifts  one  foot  after  the  other 
from  the  ground,  at  first  cautiously,  slowly,  but  soon 
with  increasing  speed.  Next,  one  foot  is  advanced  and 
the  weight  is  thrown  forwards  and  backwards  from  the 
rear  foot  to  the  advanced.  Then,  the  rear  foot  is  brought 
alongside  the  advanced.  So,  advancing  with,  say,  the 
left  and  slowly  shuffling  the  right  alongside,  progression 
starts.  Then  the  right  is  made  the  advancing  foot.  Next 
he  advances  either  foot  by  command.  Then  he  advances 
the  moving  foot  from  slightly  behind  the  stationary  to 
slightly  in  front  of  it ;  and  back  again ;  changes  the  mov- 
ing foot,  and  takes  successive  steps:  soon  he  increases 
the  number  of  steps;  lengthens  the  stride;  walks  back- 


DISORDERS  OF  MOVEMENT  259 

wards;  sideways;  and  turns.  Later,  he  walks  up  and 
down  increasingly  steep  inclines;  negotiates  steps,  at 
first  shallow,  then  deeper,  then  unequal;  walks  heel  and 
toe;  carries  weights  in  the  outstretched  hands;  runs; 
catches  a  small  medicine  ball — there  are  few  limits  to 
the  ataxic's  capacity  to  learn. 

These  movement  exercises  are  merely  a  means  to  pro- 
cure orderly  mental  action,  a  means  to  train  attention,  a 
means  to  inculcate  cerebral  control.  They  become  not 
only  useless  but  actively  injurious  when  they  are  prac- 
ticed to  the  extent  of  inducing  severe  fatigue.  Every 
movement  requires  effort.  To  avoid  fatigue  the  exer- 
cises must  involve  the  minimum  of  effort.  This  minimum 
is  achieved  by  devising  exercises  and  safeguards  so  as 
to  eliminate  fear  from  practice,  and  by  carefully  grading 
the  difficulty  and  the  duration  of  the  exercises.  The 
only  fatigue  permissible  to  the  ataxic  tabetic  should  be 
that  which  comes  from  moving  repeatedly  and  with  care. 

Certain  bodily  changes  accompany  effort.  That  most 
commonly  used  as  an  index  to  the  amount  of  effort  is 
the  pulse  rate.  To  exercise  till  the  pulse  rate  reaches 
110  per  minute  (or,  as  I  recently  saw  advocated,  140), 
is  to  retard  progress  and  to  incur  risk.  Above  a  certain 
pulse  rate,  usually  above  100  per  minute,  effort  is  not 
profitable.  That  rate  must  be  ascertained  by  observa- 
tion of  the  individual  tabetic.  When  it  is  exceeded,  the 
movements  deteriorate  and  further  exercising  wastes 
time  and  causes  futile  strain.  The  need  then  is  to  prac- 
tice not  movement  but  rest.  Five  minutes  spent  on 
rest  exercises  will  refresh  the  tabetic,  relieve  his  mental 
tension  and  reduce  the  pulse  rate  to  normal.  Then,  the 
practice  of  movement  may  usefully  recommence. 

For  every  patient,  the  most  profitable  ratio  of  move- 


260  LOCOMOTOR  ATAXIA 

ment  to  rest  exercises  should  be  determined  by  experi- 
ment; and  the  dosage  of  the  exercises  must  conform  to 
this  ratio.  This  ratio  is  not  constant ;  it  varies  from  day 
to  day  and  is  greater  at  the  beginning  than  at  the  end 
of  a  lesson  in  movement.  When  during  the.  course  of  the 
lesson  movement  does  not  improve,  general  relaxation 
should  be  given  and  then  a  fresh  start  made. 

"With  judicious  alternation  of  movement  and  of  rest 
exercises,  I  have  worked  profitably  for  two  hours  at  a 
stretch  with  a  patient.  Every  session  should  end  with 
rest  exercises  which  return  the  tabetic  to  the  physical 
state  in  which  the  session  began.  When  owing  to  pain 
or  crises,  or  other  untoward  circumstances,  the  tabetic 
is  depressed  or  fatigued,  there  should  be  more  rest  than 
movement  in  the  exercises.  Not  the  patient's  complaints, 
but  the  patient's  reactions  to  the  exercise  should  deter- 
mine the  program.  Pain  usually  diminishes  and  dis- 
appears if  the  practice  is  tactfully  conducted.  The  treat- 
ment of  the  disordered  mental  state  which  induces  ataxia 
is  also  the  treatment  of  the  disordered  mental  state  which 
magnifies  pain. 

When  the  tabetic  is  mentally  competent  to  move  coor- 
dinately  in  spite  of  all  ordinary  emergencies  in  sheltered 
life,  his  activities  should  be  broadened.  He  should  be 
taught  to  walk  freely,  confidently,  and  unaided  in  public, 
at  street  crossings,  and  at  change  of  level  and  of  surface. 
These  tasks  should,  like  all  other  tasks  of  the  tabetic, 
be  graded  in  difficulty  and  in  duration. 

The  extent  to  which  the  ataxia  will  improve  by  this 
treatment  is  always  considerable  and  often  remarkable. 
In  slight  cases  a  complete  return  to  the  preataxic  stage 
is  certain.  In  recent  cases,  cases  which  have  been  ataxic 
for  a  year  or  less,  similar  success  is  likewise  easily  at- 


DISORDERS  OF  MOVEMENT  261 

tained.  No  matter  how  long  standing  the  case  or  how 
severe  the  ataxia,  improvement  is  inevitable  if  the  pa- 
tient be  free  from  organic  mental  disease. 

I  believe  there  is  no  sane  ataxic  who  cannot  be  taught 
to  move  coordinately.  When  measurement  shows  that 
improvement  halts,  either  the  treatment  is  being  unduly 
hastened,  or  extraneous  circumstances  are  preventing 
progress.  Examination  will  at  once  disclose  if  the  treat- 
ment is  at  fault;  if  a  fundamental  posture  or  movement 
has  been  so  imperfectly  acquired  that  all  subsequent 
movements  of  which  it  forms  a  part  must  share  its  im- 
perfection. If  the  treatment  be  not  at  fault,  then  the 
tabetic's  economic  or  domestic  life  is.  Economic  condi- 
tions are  a  factor  only  in  tlie  ambulant  ataxic,  the  ataxic 
who  must  earn  his  living  while  being  treated.  The  pa- 
tient's improvement  will  depend  upon  the  extent  to 
which  we  can  mold  his  circumstances  to  his  benefit. 

Blindness,  arthropathies,  fractures,  and  muscular 
atrophy  are  not  contraindications  but  incentives  to  treat- 
ment. One  formerly  helpless  ataxic  who  demonstrated 
the  cure  of  his  ataxia  to  the  students  of  the  International 
Extension  Course,  subsequently  developed  a  Charcot 
ankle  and  knee,  and  fell  and  fractured  his  tibia;  but, 
with  some  mechanical  aid,  he  persevered  in  his  efforts  and 
manages  still  to  walk  well  enough  to  earn  his  living. 
The  possessor  of  the  fractured  tibia,  shown  in  Fig.  60, 
formerly  ataxic,  now  walks  excellently  and  pursues  his 
calling  uninterruptedly  (Fig.  95). 

The  length  of  time  necessary  to  restore  an  ataxic  to 
the  preataxic  stage  varies  with  the  individual  and  with 
the  degree  of  ataxia.  The  more  intelligent  and  indus- 
trious he  is,  the  quicker  he  learns.  The  less  ataxic  he 
is,  the  less  is  his  difficulty.  Five  lessons  may  be  adequate 


262  LOCOMOTOR  ATAXIA 

to  teach  the  rest  exercises.  If  Rombergism  alone  is  pres- 
ent little  more  teaching  is  necessary  to  procure  equilib- 
rium. 

With  cases  of  average  severity  under  constant  super- 
vision, one  month's  training  is  usually  adequate.  If  the 
ataxia  developed  suddenly  it  is  usually  quickly  removed. 
Ambulant  cases,  and  cases  long  neglected,  cases  which 
have  gradually  advanced  for  years,  take  longer.  But 
so  long  as  periodic  measurement  shows  steady  improve- 
ment, the  encouraged  tabetic  cheerfully  strives  on,  and 
progresses  as  rapidly  as  his  capacity  and  his  circum- 
stances permit. 

Permanence,  not  speed,  should  distinguish  the  cure. 
When,  by  the  treatment  of  the  mental  state,  the  tabetic 
is  made  once  more  preataxic,  he  must  be  maintained 
preataxic.  His  daily  efforts  must  be  reduced  to  his 
capacity.  He  must  avoid  occasions  of  undue  mental 
strain.  .He  must  remain  for  a  time  subject  to  the  vigilant 
medical  guardianship  which  every  preataxic  tabetic  re- 
quires. But  having  once  conquered  ataxia,  the  tabetic 
is  learned  in  the  causes  of  his  disability;  he  can  never 
again  sink  to  the  depths  from  which  he  has  emerged. 
Disturbances  in  his  gait  now  induce  in  him  not  fear 
but  study.  He  reports  his  transitory  lapse  together  with 
its  cause.  He  should  then  revert  to  the  practice  of  the 
very  simplest  movements.  A  day  or  two  usually  suffice 
to  stabilize  him  again.  When  I  returned  from  the  war, 
three  of  my  preataxic  tabetics,  who  had  long  ceased  to 
need  my  care,  reported  that  soon  after  they  heard  of  my 
departure  their  movements  became  somewhat  disor- 
ganized. This  disturbance  endured  in  one  case  for  nearly 
a  week,  in  the  others  for  several  days.  All  three  com- 
pletely recovered  by  their  own  efforts. 


DISORDERS  OF  MOVEMENT  263 

With  the  disappearance  of  the  ataxia,  pain  and  crises 
and  other  symptoms  diminish  or  disappear.  The  relief 
of  ataxia  is  merely  incidental  to  improving  the  mental 
state,  to  equipping  the  tabetic  mentally,  so  that  he  will 
be  able  to  live  with  his  irreparable  structural  changes  in 
the  minimum,  of  discomfort. 


CHAPTER  XV 

REVIEW  OF  TABES 

Afferent  nervous  system  invaded  in  disease  styled  tabes  dorsalis,  or 
locomotor  ataxia.  Disturbance  of  vegetative,  non-vegetative  and 
sensory  function.  "Locomotor  ataxia"  misleading;  "tabes  dorsalis" 
useless;  "syphilitic  neuritis  of  posterior  roots"  suggested.  Diagno- 
sis and  course  of  invasion.  Division  into  preataxic,  ataxic,  and 
paralytic  stages  a  psychological  not  an  anatomical  division.  Drug 
treatment  of  tabes.  Reciprocal  relations  of  symptoms  and  mental 
state  in  tabes,  and  interdependence  of  symptoms.  Treatment  of 
the  symptoms  through  the  mental  state.  Its  ease  and  effectiveness. 
Treatment  of  the  mental  state  through  the  symptoms.  Former 
methods,  Frenkel,  Goldscheider,  Fb'rster.  Limitations  of  Frenkel's 
method.  Development  of  present  method.  Value  of  present 
method  in  cure  and  in  prevention.  Conclusion. 

THE  first  symptoms  of  invasion  of  the  central  nervous 
system  by  the  spirochaeta  pallida,  the  spirochete  of  syph- 
ilis, usually  arise  from  implication  of  the  vegetative 
nervous  system  in  the  pupil.  The  invasion  then  spreads 
to  involve  the  vegetative  nervous  system  elsewhere,  to 
produce  lightning  pains,  or  bladder,  or  stomach,  or  other 
visceral  trouble.  At  the  same  time  it  may  affect  common 
sensory  fibers  in  the  posterior  root,  or  special  sensory 
nerves  such  as  the  optic. 

The  lesions  of  the  afferent  sensory  mechanism  in  tabes 
cause  fewer,  feebler,  and  delayed  sensory  impulses. 
These  sensory  impulses  are  of  two  kinds,  non-sentient 
and  sentient.  The  non-sentient  underlie  vegetative  and 
non-vegetative  reflex  function:  the  sentient,  perception. 

Local  disturbances  of  vegetative  reflex  function  may 
be  inconsequential  for  there  is  great  local  autonomy  in 

264 


REVIEW  OF  TABES  265 

the  vegetative  nervous  system.  But  the  cumulative  effect 
of  such  disturbances  is  to  disorganize  the  balance  of  the 
system  as  a  whole,  to  disorganize  general  vegetative 
functions,  such  as  metabolism  and  defense,  and  to  lead 
to  vagal  cataclysms,  such  as  gastric  crises. 

The  amount  of  disturbance  of  the  non-vegetative  or 
motor  reflex  function  in  tabes  varies  with  the  site,  extent, 
rapidity  of  development,  and  age  of  the  lesions.  Its 
amount  is  often  unimportant,  for  there  resides  in  the 
reflex  mechanism  a  vast  power  of  integration.  One  gets 
an  occasional  opportunity  to  realize  the  extent  of  this 
power  in  viewing  the  profound  spinal  changes  which  in 
life  produce  insignificant  manifestations  in  cases  of, 
for  example,  disseminated  sclerosis. 

Upon  the  attention  devoted  to  the  surviving  sensory 
impulses,  as  well  as  upon  the  extent  and  severity  of  the 
lesions,  depends  the  amount  of  loss  of  sensory  percep- 
tion. The  simpler  the  sensation,  the  more  accurately 
does  the  failure  of  perception  reflect  the  tabetic  destruc- 
tion. 

So  long  as  the  dominant  symptoms  arise  from  lesions 
of  the  afferent  nervous  system,  whether  vegetative,  or 
spinal,  or  cranial,  the  disease  is  now  styled  locomotor 
ataxia  or  tabes  dorsalis.  As  the  lesions  affect  not  the 
motor  but  the  sensory  system  and  as  ataxia  need  not 
and  should  not  complicate  it,  the  title  locomotor  ataxia 
is  misleading.  Excepting  habit  and  use,  there  is  as  little 
justification  for  the  continued  survival  of  the  Hippocratic 
term  tabes  dorsalis  as  for  the  persistence  of  words  such 
as  metasyphilitic  and  parasyphilitic.  The  employment 
of  meaningless,  archaic  names  for  syphilitic  infections 
of  the  central  nervous  system  leads  to  regrettable  con- 
fusion in  thinking,  in  writing,  and  in  teaching.  Revision 


266  LOCOMOTOR  ATAXIA 

and  standardizing  of  the  nomenclature  of  syphilitic  af- 
fections of  the  central  nervous  system  urgently  await 
action  by  an  influential  congress  of  neurologists. 

The  diagnosis  of  tabes  depends  upon  the  discovery 
of  the  presence  of  syphilis  and  of  signs  of  implication  of 
the  afferent  nervous  system.  The  minimum  amount  of 
implication  usually  considered  tabetic  is  implication  of 
vegetative  and  of  common  sensory  fibers,  an  implication 
which  in  the  posterior  nerve  root  occurs  as  the  result 
of  the  invasion  of  a  single  site.  In  absence  of  any.  ex 
cathedra  pronouncement  to  the  contrary,  a  disease  in 
which  a  primary  syphilitic  lesion  of  the  posterior  nerve 
roots  causes  the  dominant  symptoms  may  be  considered 
as  tabes. 

The  spirochete  attacks  no  site  exclusively,  but  invasion 
early  becoming  dominant  in  the  posterior  roots,  or  in 
the  optic  nerve,  or  in  the  cerebral  cortex,  respectively, 
tends  to  follow  a  certain  course.  The  designation  of 
the  dominant  site  somewhat  presages  the  future  of  the 
invasion.  At  any  site,  pathological  processes  are  named 
according  to  the  tissue  which  is  essentially  attacked. 
Thus,  pneumonia  remains  pneumonia  although  pleurisy 
supervenes.  The  essential  lesion  in  tabes  seems  to  be 
a  syphilitic  neuritis.  Should  it  not  be  so  styled?  Until 
we  know  whether  the  pathological  change  is  primarily 
interstitial,  as  Nageotte  contends,  or  primarily  paren- 
chymatous,  as  Stargardt  seems  to  show,  the  term 
"primary  syphilitic  neuritis  of  the  posterior  root" 
would  have  at  least  the  merit  of  describing  the  cause, 
the  dominant  site,  and  the  nature  of  most  of  the  syph- 
ilitic invasions  of  the  central  nervous  system  which  we 
now  call  tabes.  So  long  as  the  posterior  root  lesion 
produces  the  dominant  symptoms,  the  disease  still  merits 


REVIEW  OF  TABES  267 

the  description.  If  optic  neuritis,  or  encephalitis,  or 
poliomyelitis,  assumes  the  dominance  it  becomes  entitled 
to  designate  the  invasion. 

Beyond  the  facts  that  syphilis  beginning  in  the  pos- 
terior roots  tends  to  spread  first  among  them,  and  that 
the  longer  the  invasion  lasts  the  more  general  is  the 
spread,  we  cannot  foretell  its  course.  The  old  division 
of  the  disease  into  preataxic,  ataxic,  and  ''paralytic'* 
stages  is  founded  not  upon  a  pathological  but  upon  a 
psychological  basis.  The  ataxic  tabetic  is  merely  one 
whose  mental  treatment  has  been  neglected,  the  "  para- 
lytic" one  who  has  ceased  to  strive  against  his  infirmity 
and  has  surrendered  activity  rather  than  incur  the  exer- 
tion which  activity  demands. 

Before  neurologists  could  diagnose  tabes,  except  in  its 
most  aggravated  forms,  Erb  wrote  "Ueber  alle  ist  der 
Stab  gebrochen."  Brissaud  later  remarked  that  the  dis- 
ease was  growing  milder;  and  Raymond,  that  pains  and 
ataxia  were  becoming  less  severe.  Now  we  recognize 
that  about  one-seventh  of  all  cases  are  abortive:  and 
that  tabes  is  a  disease  which  is  practically  without  lethal 
power. 

As  tabes  begins  about  the  age  of  thirty-seven  and  lasts 
on  an  average  until  more  than  fifty-three  years,  the 
tabetic  has  a  life  expectancy  equal  to  at  least  two-thirds 
that  of  the  average  healthy  man.  Yet  the  force  of  tra- 
dition and  the  pessimism  of  ignorance  still  combine 
to  make  of  tabes  an  affection  as  fatal  as  cancer,  as  dread- 
ful as  leprosy.  I  know  of  two  tabetics  who  committed 
suicide ;  they  were  both  medical  men,  were  both  victims 
to  false  teaching. 

As  life  is  neither  menaced  nor  much  shortened  by 
tabes,  the  tabetic  is  an  ideal  patient  to  treat. 


268  LOCOMOTOR  ATAXIA 

Successful  treatment  of  syphilis  in  tissues  such  as 
those  of  the  central  nervous  system,  where  lesions  are 
irreparable,  lies  in  preventing  the  invasion  of  these  tis- 
sues by  aiding  the  body  to  kill  the  spirochete  ere  it 
attacks  them.  Fournier  with  all  his  skill  in  antisyphilitic 
treatment,  would  predict  from  the  banal  lesions  the  later 
occurrence  of  tabes,  and  Ehrlich  expressly  stated  that 
salvarsan  was  merely  an  adjuvant  to  the  human  defense 
substances.  And  Warthin  has  shown  post  mortem  the 
presence  of  spirochetes  in  the  central  nervous  system 
of  intensively  treated  cases  of  nerve  syphilis. 

We  cannot  by  metallic  substances,  alone,  surely  kill  the 
invading  spirochete.  Modern  therapy  pays  too  much  at- 
tention to  the  spirochete  and  too  little  to  its  host.  Our 
present  efforts  seem  not  so  much  to  reinforce  as  to 
attempt  to  replace  human  defense  by  antisyphilitic 
remedies.  These  efforts  have  not  succeeded.  Our  tasks 
now  are  to  learn  to  develop  and  strengthen  human  de- 
fense and  to  recognize  and  combat  imperfect  defense 
against  the  spirochete  before  its  evil  and  irreparable 
consequences  arise. 

The  correlation  of  biochemical  action  upon  wrhich  de- 
fense depends  is  a  function  of  the  vegetative  nervous 
system.  I  have  suggested  as  a  cause  of  imperfect 
defense,  inadequate  stimulation  of  the  vegetative  nervous 
system  owing  to  the  mildness  or  absence  of  the  pretabetic 
lesions.  Perhaps  our  haste  to  banish  ordinary  syphilitic 
lesions  by  drugs  may  contribute  to  increase  the  frequency 
of  nervous  syphilis. 

The  importance  of  mental  stress  in  conducing  to  tabes 
lies  in  the  disturbance  by  mental  stress  of  the  control 
of  the  vegetative  system  over  the  chemical  confederacy, 
The  progressive  nature  of  spinal  tabes  and  the  abortive 


REVIEW  OF  TABES  269 

tendency  of  optic  tabes  are  partly  clue  to  the  implication 
of  the  vegetative  nervous  system  in  the  first  and  to  its 
immunity  in  the  second.  Neither  the  transient  inhibition 
of  the  growth  of  the  spirochete  nor  the  indiscriminate 
general  excitation  of  the  vegetative  nervous  system, 
exerted  by  the  metallic  substances  which  we  now  employ 
as  antisyphilitic  remedies,  but  the  development  and  rein- 
forcement of  the  natural  human  defense  against  the 
spirochete  by  well  directed  stimulation  of  the  vegetative 
nervous  system,  with  specific,  unorganized,  chemical  sub- 
stances, such  as  vaccines,  will  ultimately  afford  the  cure 
for  which  we  seek.  This  cure  is  now  unknown  to  us, 
mainly,  I  think,  because  its  quest  has  been  neglected  in 
favor  of  the  pursuit  of  the  philosopher's  stone  of  medi- 
cine, the  drug  w^hich  will  totally  destroy  the  spirochete 
in  every  human  tissue. 

In  default  of  any  agent  of  proven  power  to  cure  or  to 
arrest  the  syphilitic  invasion,  we  are  forced  to  treat,  not 
the  structural  results  of  that  invasion,  but  the  tabetic's 
reaction  to  them.  For  this  purpose  we  have  examined 
the  various  symptoms  to  determine  the  relative  impor- 
tance of  the  structural  and  psychic  elements  in  their 
production;  and  we  have  studied  the  mental  state,  to- 
gether with  the  influences  favorable  and  unfavorable  to 
mental  action.  We  found  that  the  mental  state  and  the 
tabetic  symptom  are  reciprocally  related  and  that 
through  the  mental  state  the  symptoms  are  interdepen- 
dent. As  a  necessary  corollary  to  these  relations,  im- 
provement of  the  mental  state  relieves  the  tabetic  symp- 
toms and  relief  of  any  tabetic  symptom  improves  the 
mental  state  and  alleviates  the  other  symptoms. 

The  principles  on  which  I  have  founded  the  treatment 
of  the  mental  state  are,  I  think,  basic.  The  method  I 


270  LOCOMOTOR  ATAXIA 

have  described  of  applying  these  principles  is  effective. 
But  many  other  measures  of  training  in  cerebral  control 
may  be  devised.  Any  mental  task  neither  too  complex 
nor  too  novel,  whose  performance  can  be  checked  and 
measured,  which  can  be  repeated  both  unchanged  and 
with  regulated  complexity,  will  prove  serviceable.  Nor 
need  the  instruments  I  have  mentioned  be  used.  These 
are  of  value  where  the  similarly  sick  congregate,  for 
they  simplify  work  and  permit  greater  accuracy  in  treat- 
ment. But  a  hand  mirror  may  take  the  place  of  the 
cephalograph  and  of  the  modified  perimeter.  Lines 
chalked  on  the  wall  or  marked  by  tapes  may  guide  the 
eyes  in  the  direction  and  extent  of  the  movement.  Strik- 
ing out  certain  vowels  or  consonants  with  a  pencil,  from 
the  columns  of  a  daily  newspaper,  will  afford  a  useful 
substitute  for  reckoning  tests.  No  appliances  are  needed. 
The  one  requisite  is  the  interest  of  the  physician. 

Properly  directed  treatment  brings  immediate  results. 
The  effect  of  every  hour's  instruction  is  evident  in  im- 
provement. Skill  is  less  necessary  than  systematization 
in  the  treatment.  From  the  outline  I  have  given  every 
physician  can  effectively  treat  a  tabetic.  Every  physi- 
cian can  become  a  center  round  which  the  incipient 
tabetics  may  gather  for  that  guidance  and  training  which 
will  alleviate  and  may  arrest  the  disease.  No  extensive 
experience  is  necessary.  An  intelligent  study  of  a  single 
case  will  fortify  the  physician  against  most  of  the  prob- 
lems he  may  subsequently  encounter.  And  when  a 
difficulty  arises,  consideration  of  it  in  association  with 
the  essential  principles  which  govern  the  treatment  will 
provide  a  solution. 

As  motor  disturbance,  especially  ataxia,  is  to  most 
tabetics  the  chief  burden  of  the  disease,  and  as  the  prob- 


REVIEW  OF  TABES  271 

lem  of  voluntary  movement  particularly  interested  me,  I 
used  the  treatment  of  ataxia  to  exemplify  in  detail  the 
relief  and  cure  of  a  tabetic  disability. 

Disturbance  of  voluntary  movement  is  neither  an  im- 
mediate nor  an  inevitable  nor  a  direct  effect  of  the 
tabetic  lesions.  It  is  an  effect  in  which  the  tabetic  lesions 
play  a  part  but  in  which  deterioration  of  the  mental  state 
plays  the  major  role.  So  long  as  the  mental  processes 
of  the  tabetic  reflect  with  sufficient  intensity  his  desire 
to  move,  the  structural  changes  remain  masked.  When 
the  mental  state  deteriorates  to  a  level  at  which  orderly 
movement  is  no  longer  possible,  the  resulting  ataxic 
movement  is  compounded  of  the  desire,  the  mental  state, 
and  the  reflex  defect. 

Ataxia,  which  is  in  large  measure  merely  a  result  of 
deterioration  of  the  mental  state,  unfortunately,  has 
hitherto  been  the  first  sign  to  induce  the  physician  to 
treat  the  mental  state.  The  nature  of  the  symptom  provi- 
dentially directed  the  mode  of  treatment.  But  the 
physician  tried  to  bring  order  out  of  ataxic  movements 
without  realizing  that  his  real  purpose  wTas  to  bring 
order  to  chaotic  mental  processes.  Hence,  to  his  own 
hindrance  and  to  the  patient's  detriment,  the  physician 
was  ignorant  of  the  help  which  lay  to  his  hand. 

The  apostle  of  the  ataxic  tabetic  is  Frenkel.  To  his 
genius  we  owe,  if  not  the  discovery,  at  least  the  practical 
application  of  motor  therapy. 

Since  1897,  he  and  his  disciples — greatest  among  whom 
,is  Forster — with  untiring  persistence  and  admirable 
skill  have  striven  to  educate  medical  opinion  on  behalf 
of  the  tabetic.  To  Frenkel  and  his  co-workers,  medicine 
owes  the  present  universal  recognition  that  the  ataxic. 
can  be  substantially  aided.  Groldscheider,  1899,  in  a 


272  LOCOMOTOR  ATAXIA 

book  of  a  few  score  of  pages,  a  masterpiece  of  clear 
thinking  and  of  orderly  exposition,  systematized  Fren- 
kel's  method  and  first  clearly  taught  that  upon  the  per- 
fection of  the  primary  qualities  of  direction,  extent  and 
rhythm  depends  the  perfection  of  the  simple  movement 
which  is  the  source  of  the  perfection  of  all  complex  move- 
ments. To  Frenkel,  Goldscheider,  and  Forster  is  due 
practically  all  the  effective  aid  hitherto  given  to  the 
tabetic. 

In  common  with  most  who  practiced  the  Frenkel 
method,  I  was  often  disappointed  with  its  results.  Al- 
though by  its  aid  many  ataxies  could  laboriously  be 
brought  to  a  fair  degree  of  motor  efficiency,  many  could 
not.  The  latter  might  acquire  some  dexterity  in  moving 
in  the  recumbent  posture,  and  they  might  slightly  im- 
prove in  walking,  but  they  then  improved  no  further. 
Such  were  the  timorous  and  those  who  by  the  results  of 
their  efforts  were  not  encouraged  to  persevere.  Failing, 
vision  and  arthropathy  were  stated  by  Frenkel  to  contra- 
indicate  his  treatment.  I  never  succeeded  by  the  Frenkel 
method  in  educating  an  average  ataxic  to  walk  without 
aid.  Nor  does  Frenkel  state  that  such  success  is  prob- 
able. The  freedom  of  the  blind  tabetic  from  ataxia  and 
the  complete  recovery  from  ataxia  which  may  spontane- 
ously follow  the  establishment  of  blindness,  led  me  to 
teach  ataxies  to  move  blindfolded  in  the  hope  that  the 
tabetic  would  thereby  attain  greater  perfection  in  move- 
ment. One  of  my  early  patients  was  an  ataxic  who  had 
derived  great  benefit  from  Professor  Frenkel 's  personal 
care,  but  who  being  seated  one  night  in  a  restaurant 
when  the  lights  suddenly  failed,  soon  found  himself 
sprawling  helplessly  on  the  floor.  Blindfolded  teaching 
promised,  therefore,  more  perfect  and  more  useful  move- 


REVIEW  OF  TABES  273 

ment.  This  promise  has  not  only  been  fulfilled,  but 
blindfolded  moving  has,  moreover,  proved  easier  to  learn 
than  moving  by  vision. 

My  former  colleague,  Professor  Wachsmann,  without 
knowledge  of  my  work,  also  conceived  the  idea  of  teach- 
ing ataxies  to  move  blindfolded.  I  demonstrated  to  the 
International  Extension  Course  in  1913,  together  with 
two  of  my  own  cases,  a  tabetic  whom  he  had  thus  taught 
to  move  excellently. 

To  combat  the  depression  which  prolonged  practice  in 
the  recumbent  posture  caused,  to  obtain  an  easy  transi- 
tion from  movements  in  stationary  attitudes  to  progres- 
sion, and  to  strengthen  and  correlate  the  head  and  trunk 
movements,  I  introduced  creeping  and  kneeling  exercises. 
To  insure  easy  movement,  I  next  used  passive  exercises 
to  remove  muscular  constraint.  To  calm  and  to  rest  the 
excited,  fatigued  tabetic,  after  movement,  I  found  that 
these  passive  exercises  together  with  breathing  exercises 
were  effective. 

The  success  of  the  rest  exercises,  not  merely  in  tabes 
but  also  in  cases  of  muscular,  vascular,  and  mental  ten- 
sion (Sorapure  and  Maloney),  in  spasmodic  muscular 
affections  of  functional  origin  (Abrahamson  and  Pollen), 
and  in  chorea  (Grossman),  and  observations  of  the 
effect  of  fatigue  and  fear  upon  ataxia,  emphasized  the 
mental  factor  in  ataxia  to  a  degree  which  I  had  hitherto 
not  realized.  Then  there  quickly  followed  the  systematiz- 
ing of  the  treatment :  its  application  not  only  to  the  relief 
of  ataxia,  but  also  to  the  relief  of  other  tabetic  symp- 
toms; next  its  use  to  prevent  these  symptoms;  and 
finally  its  employment  in  the  treatment  of  syphilitic 
neurasthenia. 

Those  with  fracture,  with  arthropathy,  with  muscu- 


274 


LOCOMOTOR  ATAXIA 


lar  atrophy  and  with  failing  vision  ai'e  in  as  urgent 
need  of  treatment  as  their  more  fortunate  fellows  and 
their  special  disabilities  are  rather  incentives  than 
contraindications  to  treatment. 

As  a  cure  of  ataxia  the  treat- 
ment I  have  outlined  has  proved 
speedy  and  efficacious,  not  mere- 
ly in  my  experience  but  in  that 
of  others.  Dr.  Sorapure,  Dr. 
Grossman  and  Dr.  Wolf  have 
demonstrated  to  various  med- 
ical societies  former  ataxies 
whom  they  have  by  this  method 
taught  to  walk  confidently  and 
well.  Drs.  Grossman  and 
Wolf  have  published  some  of 
their  cases.  Dr.  Grossman 
and  I  have  further  publicly  dem- 
onstrated cases  first  before  and 
again  after  treatment  had  re- 
moved the  ataxia.  The  amount 
of  improvement  which  must  oc- 
cur before  an  ataxic,  blindfold- 
ed and  unaided,  can  successfully 
undergo  the  ordeal  of  a  public 
demonstration  will  be  appreci- 
ated by  all  who  have  any  ex- 

X 

perience  of  the  ataxic  tabetic. 

Of  the  value  of  this  treatment  in  preventing  ataxia  I 
have  much  less  experience.  But  no  case  under  the  care 
of  any  of  the  physicians  who  have  used  this  method  or 
under  my  care  has  developed  ataxia.  Economic  condi- 
tions may  force  the  tabetic  to  continue  to  toil  beyond  his 


FIG.  97. — This  patient  suf- 
fers from  the  ununited 
fracture  of  the  tibia 
shown  in  Fig.  60,  but  in 
spite  of  that  defect  he 
was  successfully  cured 
of  ataxia.  (Grossman.) 


REVIEW  OF  TABES  275 

strength;  business  reverses  may  sway  the  tabetic  more 
powerfully  than  therapy  can  counterbalance ;  family  dis- 
sensions, accidents,  chills,  or  other  disadvantageous  hap- 
penings may  impose  a  limit  on  the  success  of  the  therapy; 
and  ataxia  may  develop.  Regret  in  such  circumstances 
will  be  softened  by  time,  the  time  by  which  the  preataxic 
stage  has  exceeded  its  average  duration;  by  the  cer- 
tainty that  the  disaster  can  be  speedily  retrieved;  and 
by  the  knowledge  that  its  memory  will  ever  after  exert 
a  salutary  restraining  influence  upon  the  tabetic  and 
upon  his  associates. 

The  treatment  of  the  ataxic  tabetic  differs  in  no  essen- 
tial detail  from  the  treatment  of  the  preataxic  tabetic: 
and  the  treatment  of  the  preataxic  tabetic  is  identical 
with  that  of  the  syphilitic  neurasthenic.  If  physicians 
will  only  realize  the  unity  of  purpose  which  governs  the 
treatment  of  these  conditions,  much  of  the  burden  may  be 
lifted  from  the  shoulders  of  the  victims  of  syphilis  of 
the  central  nervous  system. 

The  results  are  more  gratifying  than  any  I  know  in 
the  realm  of  therapy  outside  of  surgery.  To  raise  the 
hopeless  bedridden  tabetic;  to  make  him  walk  again;  to 
place  him  once  more  not  only  in  relation  to  but  in  com- 
petition with  his  normal  fellows;  to  arrest  the  wretched 
tabetic's  progress  in  ataxia;  to  lead  him  back  to  con- 
fidence, to  stability,  to  ordered  movement ;  and,  greatest 
of  all,  to  prevent  ataxia,  to  safeguard  the  tabetic  from 
the  misery  with  which  his  ignorance  soon  endows  his 
disease — these  services  are  not  only  a  duty  which  the 
medical  man  owes  to  his  patient,  they  are  services  which 
humanity  claims  as  a  right. 

The  victims  of  tabes  are  the  spirochete's  prey  among 


276  LOCOMOTOR  ATAXIA 

the  intellectual.  No  country  can  afford  to  allow  their 
valuable  lives  to  be  frittered  away  for  lack  of  a  few 
weeks  of  systematic  treatment.  In  any  community  their 
number  is  seldom  sufficient  to  arouse  public  interest  to 
the  point  necessary  for  action  on  their  behalf.  The 
founding  of  a  small  national  hospital  for  their  treatment 
and  for  their,  further  study,  would  be,  indeed,  beneficent. 


BIBLIOGRAPHY 

ABADIE,  J.     Constitution  d'un  schema  semiologique  du  tabes, 

Rev.  neurol.,  1911,  p.  787. 
ABRAHAMSON  AND  POLLEN.     On  the  Treatment  of  Spasmodic 

Muscular  Affections   of   Functional   Origin   by  Maloney's 

Method.     Paper  read  before  the  New  York  Neurological 

Society,  April,  1914. 
APELT.     Die  Bedeutung  cytologischer  Untersuchungen  der  Cere- 

brospinalfliissigkeit  fiir  die  Neurologie,  Monatschr.  f.  Psy- 

chiat.  u.  Neurol.,  No.  20.     See  also  Nonne's  Syphilis  und 

Nervensystem. 
BAILEY,  PEARCE.     The  Effect  of  Early  Optic  Atrophy  upon  the 

Course  of  Locomotoj-  Ataxia,  Med.  Rec.,  Nov.  14,  1896. 
BARKER,  LEWELLYS  F.     Monographic  Medicine,  New  York,  D. 

Appleton  &  Co.,  1916,  vol.  iv. 
BEAUSSART.     Tabetiques  et  paralytiques  generaux  conjugaux  et 

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WILLCOX.     Quoted  by  Mclntosh,  Fildes,  etc.,  loc.  cit. 
WILSON,  S.  A.  K.     The  Pathology  of  Two  Cases  of  Tabetic  Amy- 

otrophy.    Rev.  Neurol.  and  Psych.,  Edinburgh,  Aug.,  1911, 

pp.  401-418. 
WOLF,  H.  F.     The  Symptom  Ataxia,  Its  Successful  Treatment. 

N.  Y.  Med.  J.,  Sept.  9,  1916. 
The   Treatment  of  Locomotor   Ataxia  by  the  Maloney 

Method,  ibid.,  July  21,  1917. 


INDEX 


Abducens  lesions  in  tabes,  13 
Abrahamson  and  Pollen,  treatment 

of  spasmodic  muscular  af- 
fections, 273 
Accessibility  of  tissues   to  spiro- 

chete,  5 

Achilles  jerk,  33 
Acquired     immunity     to      spiro- 

chetes,  138-139 
Acute  ataxia,  72,  73 
Adrenalin,  action  of,  136 
effect  of,  136 
use  of,  to  prevent  lesions  after 

salvarsan,  146 
Age,  at  death  in  tabes,  163,  164 

at  onset  of  tabes,  163 
Aids  to  stability,  mechanical,  240- 

241 

Algesimeter,  48 
Algometer,  48 
"All  fours"  posture,  249 
Alternative  reflex  paths,  25,  26 
Amyl  alcohol,  site  of  lesions,  14 
Analgesia,  52,  53 
Analgesics,  218 
Anatomical  basis  of  tabetic  signs, 

152 

Ankle  exercises,  255 
Anterior  horn  cell  lesions  in  tabes, 

13 

Antisyphilitic  substances,  166 
Anxiety  neurosis  in  tabes,  177 
Argyll-Robertson  pupil,  119,  153 
Arm  jerks,  33 
Arsenic,  166,  170,  172 
Arsenical  preparations,  172 
Arthropathies,  137 


Asynergia,  44 
Ataxia,  acute,  72,  73 

amount  of  improvement  in,  fol- 
lowing blindness,  103 
an  emotional  expression,  82 
and  blindness,  relation  of,  104 
and  mental  state,  77 
and  postural  loss,  70 
and  reflex  loss,  70 
and  sensory  loss,  70 
and  tabetic  lesions,  73,  74 
blindfold  treatment,  advantages 

of,  272-273 
co-efficient  of,  78 
course  of,  71,  72 
definition  of,  69 
disappearing       in       blindness, 
Abrahamson's  case,  98,  99 

Benedikt's  case,  97 

Benenati's  cases,  98 

Bouchaud's  case,  97 

Forster's  cases,  98 

Inglerans*  cases,  97,  98 

Leri's  case,  99 

Martin's  case,  97 
duration  of  treatment  of,  261- 

262 

extent  of  improvement,  260,  261 
following  blindness,  101 
Frenkel's  method  of  treatment, 

271-272 

index  of  mental  state,  186 
liability  to,  78 
mainly  a  spatial  defect,  81 
mechanism  of,  83 
onset  of,  71 
palliation  of,  229 


287 


288 


INDEX 


Ataxia,  permanency  of  cure,  262 
preceding  blindness,  96-104 
preliminary  treatment  of, 

a.  mental,  244-247 

b.  muscular,  245 
prevention  of,  212,  228 
recording  of,  228 

role  of  the  several  parts  of  the 

muscular  apparatus  in,  69 
theories  of,  69 
treatment  in  blindness,  261 
variations  in,  74 
Ataxic  attitude,  229 
complexes,  77 
foot,  mechanics  of,  230-231 
moment,  73 
threshold,  78 
Atropin    in    treatment    of    vago- 

tonia,  191 
Attacking     force     of     persisting 

spirochete,  11 

Attention,  role  in  sensory  percep- 
tion, 47,  48,  49 
Attitude.     See  posture 
Auditory  nerve.    See  cochlear 

Back  braces,  240-241 
Baths,  204 

Beaussart's    nerve    spirochete    se- 
ries, 9 

Bedridden  tabes,  determining  fac- 
tors in,  161,  162 
Beliere's   nerve  spirochete   series, 

8 

Benedikt's  "law,"  94 
advocates  of,  95 
Dejerine  and  Martin  on,  95 
opponents  of,  95 
Blind  tabetics,  postural  sense  of, 

59 

sensory  perception  in,  59 
Blindfold  movement,  247 
Blindfolding,  mask  for,  247 
to  focus  attention,  247 


Blindness,    amount    of    improve- 
ment of  ataxia  in,  103 

and  ataxia,  96-104 

and  ataxia   developing  simulta- 
neously, 101 

and  ataxia,  relations  of,  104 

and  deafness,  105 

and  pain,  105 

effect  of  drugs  on,  mercury,  94 
mescalin,  89 
salvarsan,  94 

following  ataxia,  9 

frequency  of,  91,  94 

improvement  in,  93,  94 

influence  upon  ataxia,  101 

influence  upon  mental  state,  102 

preceding  ataxia,  92 

rate  of  development,  92 

treatment  of,  223 
Boot,  tabetic,  238 
Braces,  back,  240-241 

foot,  237 

knee,  240-241 
Breathing  exercises,  196 
Burr,  cause  of  death  in  tabetics,  11 

.  Cardiac  diseases  in  tabes,  164 
Cardiovascular  and  nervous  syph- 
ilis, 11 
Causal    relation    of    syphilis    to 

tabes,  2 

Causes  of  death  in  tabes,  11,  164 
Causes  of  imperfect  defence,  149 
Central  nervous  system,  determi- 
nants of  invasion,  12 
Centers  of  vegetative  activity,  119 
Cephalograph,  205 
Cephalograph,     measurement     of 

swaying,  65 
Cerebellum  lesions  in  tabes,  13 

functions  of,  30,  31 
Cerebral  theory  of  ataxia,  69,  71 
Cerebrospinal  fluid  in  tabes,  152 
Charcot  joints.    See  arthropathies 


INDEX 


289 


Chemical  action  and  defense,  145 
Cocain  in  gastric  crises,  220 
Cochlear  nerve,  113 
Complex  movements,  training  in, 

255 

Complexes,  ataxic,  77 
Complexes,  fear,  177 
Constitutional  influences  in  nerve 

syphilis,  12 

Cortical  lesions  in  tabes,  12,  13 
Cortical  motor  reactions,  42 
Course  of  ataxia,  71,  72 
Course  of  optic  atrophy,  87 
Creeping,  257 

Creeping,  knee-guards  for,  256 
Crises,  bladder,  129 

duration  of,  131 

gastric,  127 

genital,  130 

ocular,  127 

pain,  127 

rectal,  129 

Crises  and  mental  state,  130-131 
Cystitis  in  tabes,  164 

Deafness   and  mental   state,  114- 

115 

Deafness,  daily  variations  in,  115 
detection,  113 
psychic,  113 
tabetic,  113 
treatment  of,  224 
Death  in  tabes,  163,  164 

causes  of,  11,  164 
Death  rate  among  tabetics,  164 
Deep  reflexes,  32,  33 
Defense,   causes   of  imperfection, 

149 
effect    of    mental    strain    upon, 

148-149 

mechanism  of,  136 
substances,  existence  of,  144-145 
Dejerine,  frequency  of  root  lesions 
in  paresis,  12 


Delayed   perception  from  incom- 
plete lesions,  52 
Depression  in  tabes,  178 
Determinants  of  invasion  of  cen- 
tral nervous  system,  12 
of  site  of  initial  invasion,  15 
of  spread  of  invasion,  16 
Development   of  ataxia,   mechan- 
ism of,  80 

Diagnosis  of  tabes,  153 
Diagnosis,   precipitant  of  ataxia, 

194 

Diplopia,  cure  of,  207 
examination  of,  107 
frequency,  mechanism,  causes 

of,  105 

treatment  of,  215 
Direction,  training  in,  251 
Direction  of  movement,  threshold 

of,  58 

Discovery  of  tabes,  1 
Dislocations,  35 

Distribution  of  sensory  loss,  52, 53 
of  spirochete,  13,  14 
of  postural  loss,  58 
Dosage  of  exercises,  207 
of  movement  exercises,  248 
of  postural  exercises,  256 
Drainage  theory  of  reflex  action, 

28 
Drug  treatment,  physical  factors 

in,  174 

psychological  factors  in,  174 
Duchenne,  discovery  of  tabes,  1 

on  diagnosis  of  tabes,  155 
Duration  of  pretabetic  period,  156- 
158 

Edinger's  fatigue  theory,  14,  15 

Effort  and  movement,  76 

Eighth  nerve.    See  vestibular  and 

cochlear 
Electricity,  251 
Equilibration,  center  of,  31 


290 


INDEX 


Erb's  nerve  spirochete  series,  9 
Ergot,  site  of  lesions,  14 
Exciting  cause  of  tabes,  2 
Exciting  organism  of  tabes,  5 
Exercises,  ankle,  255 

breathing,  196 

eye,  206 

graduation  of,  207 

head,  205 

head  and  neck,  253 

hip,  254 

knee,  254 

passive,  198-199 

resistance,  251 

rest,  196-204 

trunk,  253 
Exner's     operation     for     gastric 

crises,  221 
Eye  exercises,  206 

Facial  lesions.    See  seventh 
Factors   determining  response  to 

stimuli,  49 

Factors  determining  fate  of  sen- 
sory images,  48 
Factors  in.  a  voluntary  movement, 

76 

Factors  in  posture,  62 
Factors  in  pretabetic  period,  156 
Factors  of  muscle  tone,  31 
Fatigue  in  tabes,  176 
Fatigue  theory,  Edinger,  14,  15 
Fear  and  movement,  68 

and  posture,  68 

complexes,  177 

in  tabes,  176,  177 
Feet,  tabetic,  229,  230 
Fifth  nerve  lesions,  110 
Flat  foot,  34,  229,  230 
Foot,  aims  in  bracing,  237 
Foot  blisters,  231 
Foot,  bracing,  237 
Foot  cast,  of  foot  in  action,  232 

of  foot  at  rest,  232 


Foot,  structural  changes  in  tabetic, 

236 
Forster's    operation    for    gastric 

crises,  220-221 
Frenkel's  method,  272 
Frequency  of  blindness,  91,  92 
of  muscular  atrophy,  17 
of  optic  atrophy  in  tabes,  12 
of  paresis    following   optic 

atrophy,  12 
of  peripheral  neuritis  in  tabes, 

12 
of  posterior  root  lesions  in  optic 

atrophy,  12 
Frequency    of   tabetic    signs    and 

symptoms,  Abadie,  151 
Leimbach,  151 
Sarbo,  151 
Schaffer,  151 

Function,  cerebellar,  30,  31 
Function  of  muscle  spindle,  24 

Gastric  crises,  cocain  in,  220 
measurement  of,  218 
mental  treatment  of,  219 
morphin  in,  220 
nature,  127 
novococain  in,  220 
palliative  treatment  of,  219 
prevention  of,  219 
rest  in,  219 

root  section  in,  220-221 
General    paresis    following    optic 

atrophy,  12 
General  paresis,  frequency  of  root 

lesions  in,  12 
Genu  recurvatum,  34 
Glands,    endocrinous    or   internal 

secreting,  135 
Goldscheider's      instrument      for 

measuring  posture,  57 
Gordon  Holmes,  cortical  lesions  in 

tabes,  12,  13 
Grossman,  cure  of  ataxia,  274 


INDEX 


291 


Hallucinatory  conditions  in  tabes, 

178 
Head  exercises,  205 

and  neck  exercises,  253 
Hearing,  mechanism  of,  112 
Henderson,  psychoses  of  tabes,  178 
Hip  exercises,  254 
Hitzig's  accident  theory,  15 
Hormones,  nature  and  action,  135 
Horsley     and     Slinger,     postural 

sense  in  blind,  59 
Hypochondria  in  tabes,  178 
Hypotonia,  effect  on  joints,  34 

result  of  muscle  stretching,  34 

Immunity    of    tissues    to    spiro- 
chetes,  132-139 

Imperfect  sensation  from  incom- 
plete lesions,  52 

Incubation  period.    See  pretabetic 
period 

Infection  general  in  syphilis,  5 

Influence  of  spirochete's  distribu- 
tion, 14 

optic  on  spinal  tabes,  16,  17 
nerve    lymphatics    upon   spiro- 
chete's distribution,  14 

Instruments  for  measuring  stimuli, 
48 

Integration,  spinal,  28 

Internal  secreting  glands,  135 

Involuntary     micturition,      treat- 
ment of,  222-223 

lodids,  170 

Isolation  in  treatment,  210 

Isolation  of  tabes,  177 


James'  theory,  195 
Jaw  jerk,  33 
Jendrassik,     cortical 

tabes,  12 
Joint  braces,  240-241 


lesions     in 


Knee,  braces,  240-241 

exercises,  254 

Knee-guards  for  creeping,  256 
Knee-jerk,  a  reflex  act,  32 

briskness  of,  32 

eliciting,  32 

extent  of,  32 

fatiguability  of,  32 

influence  of  flexor  tone  of,  32 

nature  of,  32 

normal  variations  of,  32 

pathological  changes  of,  33 

reinforcement  of,  32 
Kneeling,  249,  258 

Law  of  relays,  39 

Law  relating  blindness  and  ataxia, 
104 

Lesions  of  basal  nuclei  in  tabes,  13 

Lesions.     See  tabetic  lesions 

Lesions,  sequence  of,  16 

Lethality  of  tabes,  164 

Liability  of  neuron  to  invasion,  15 

Liability    to    syphilis    of   central 
nervous  system,  12 

Light  perception,  measurement  of, 
89 

Lightning  pains,  126.    See  pains, 
lightning 

Loss  of  pinprick  pain,  52 
of  postural  sense,  58 
of  pressure  pain,  124-125 
of  tactile  sense,  53 
of  temperature  sense,  53 
of  vibration  sense,  54 
of  vision,  course  of,  88 
of  vision,  degree,  88 
of  vision,  measurement  of,  88 

Lymphatics,  influence  upon  site  of 
attack,  14 

Lymphatics  in  optic  nerve,  13 

Lymphatics  in  posterior  root,  13 

Macdougall's  drainage  theory,  28 
Maintenance  of  posture,  62 


292 


INDEX 


Manic  depressive  insanity  in  tabes, 

178 
Marie,    cause    of    posterior    root 

lesion,  19,  20 
Mask  for  blindfolding,  247 
Masking  of  reflex  defect  by  cor- 
tical action,  43 
Massage,  257 
Matsunaga,  cardiac  disease  among 

tabetics,  11 
Measurement  of  light  perception, 

89 

of  loss  of  vision,  88 
of  mental  state,  179 
of  postural  loss,  56 
of  swaying,   cephalograph,   65 
Mechanical  aids  to  stability,  240- 

241 

Mechanism  of  hearing,  112 
of  micturition,  131-132 
of  pupillary  movement,  118 
of  Rombergism,  57 
of  suppression   of  postural 

images,  57,  58 
of  voluntary  movement,  42 
Melancholia  in  tabes,  178 
Mental  factor  in  muscular  weak- 
ness, 37 

Mental    training    through    move- 
ment, 204-207 
Mental  state  and  ataxia,  77 
and  crises,  128 
and  deafness,  114-115 
and  movement,  76 
and  pain,  130-131 
and  virility,  130 
deterioration  of,  183-1^4 
effect  of  symptoms  on,  184 
influence  of  posture  upon,  62 
influence  upon  signs  of,  185 
influence    upon    symptoms    of, 

184 

measurement  of,  179 
principles  of  treatment  of,  188 


Mental  state,  relief  through  treat- 
ment of  eye  symptoms  of, 
215 
Mental  strain,  effect  on   defense, 

148-149 

Mental  stress  and  tabes,  146-147 
Mercury,  166,  170 

failure  of,  in  treatment  of  optic 

atrophy,  169 
modes  of  administration  of,  in- 

gestion,  170 
inhalation,  171 
injection,  171 
inunction,  170-171 
Meyer,  psychoses  of  tabes,  178 
Micturition,  involuntary,  mechan- 
ism of,  133 
voluntary,   mechanism   of,   131- 

132 

Mobility  of  joints,  34,  35 
Morel  Lavallee's  nerve  spirochete 

series,  9 

Morphin  in  gastric  crises,  220 
Motor  nerve  lesions  in  tabes,  13 
Motor  reactions,  cortical,  42 

reflex,  43 

Movement,  after-images  of,  79 
and  effort,  76 
and  mental  state,  76 
and  posture,  248 
critique  of,  79 
Movement  exercises  in,  recumbent 

posture,  248 
"all  fours,"  249 
kneeling,  249 
standing,  249 
Movement     exercises,     order     of 

using,  252 
pulse  in,  259 
Movement,    factors   in   perfection 

of,  75 

Movement  in  fear,  68 
Movement,  preliminary  stabilising 
of,  248-249 


INDEX 


293 


Movement,  role  of  vision  in  learn- 
ing, 75 

Movement,  threshold  of,  57 
Movements,  complex,  training  in, 

455 

Movements,  creeping,  257 
kneeling,  258 
simple,  251 

cardinal  qualities  of,  251 
training  in  strength,   251 
walking,  258 

Moving  by  visual  direction,  245 
Muscle  spindle,  23 

tone  center,  31 

Muscular  apparatus,   sensory   re- 
ceptors, 54,  55 
Muscular  atrophy,   frequency   of, 

17 

Muscular  weakness,  factors  in,  37 
Myelin  sheath,  degeneration  of,  52 
function  of,  52 

Nageotte,    tabetic    posterior    root 

lesion,  21 
Nature   of  posterior  root  lesions, 

21 
Nerve   lymphatics,   spirochete    in, 

13 
Nerve  relays,  cerebellar,  30 

sentient,  45,  47 
Nerve    spirochete    series,    Beaus- 

sart's,  9 
Beliere's,  8 
Erb's,  9 

Morel   LavalleVs,   9 
Nervous    lesions,    specific    spiro- 
chete, 5 
Neurasthenia,  syphilitic,  153 

treatment  of,  190,  191,  192 
Noguchi,   discovery   of   spirochete 

in  tabes,  4 
Nonne,     peripheral     neuritis     in 

tabes,  12 
Normal  swaying,  62,  63 


Normal  and  morbid  swaying,  dif- 
ferentiation, 64,  65 
Nourishing  the  tabetic,  203 
Novocain  in  gastric  crises,  220 
Nucleinic  acid,  175 

Occupation,   adjustment  of  tabet- 
ic's, 211-212 
Occupational   incidence   of  tabes, 

147 
Occupational   influences  in   nerve 

syphilis,  12 

Occurrence  of  syphilis  in  tabes,  2 
Oculomotor  lesions  in  tabes,  13 
Onset  of  ataxia,  71 
Opiates.     See  morphin 
Oppenheim,  peripheral  neuritis  in 

tabes,  12 

Optic  atrophy,  87 
course  of,  87 

effect  on  spinal  tabes,  16,  17 
frequency  of  posterior  root  \3- 

sions  in,  12 
nature,  87 

ophthalmoscopic  findings,  87 
results  of,  88 
treatment  of,  223 
Optic  atrophy  and  diplopia,  107 
Optic  atrophy  followed  by  general 

paresis,  frequency  of,  12 
Optic  nerve,  atrophy  of,  87 
lymphatics,  13 

site  of  amyl  alcohol  lesions,  14 
Optic  tabes,  cause  of  abortive  na- 
ture of,  150 

influence  on  spinal,  16,  17 
nature  of,  87 

OIT    and    Rows,    posterior    root 
lymphatics,  13 

Pain,  an  emotional  outlet,  217 

and  mental  state,  216 
Pain  crisis,  treatment  of,  218 
Pain  in  treatment  of,  217 


294 


INDEX 


Pain,    lightning,    distribution    of, 

126 

cause  of,  126 
nature  of,  127 
occurrence  of,  126 
onset  of,  126 

Pain,  measurement  of,  216 
Pain  pressure,  relation  to  vegeta- 
tive  nervous   system,    120- 
124 

Pain  pinprick,  loss  of,  52,  53 
Pain,  reaction  to,  216 
Pain,  subacute,  treatment  of,  218 
Pain,  treatment  of,  217-218 
"Paralytic"  period,  161 

nature  of,  183-184 
Paranoia  in  tabes,  178 
Paresis.     See  general  paresis 
Paresthesia,  53 
Passive   muscular   exercises,    198- 

199 

Peripheral  neuritis  in  tabes,  fre- 
quency of,  12 
Persisting  spirochete,  types  of,  11 

attacking  force  of,  11 
Plaster  casts  of  foot,  232 
Pneumograph,  204 
Pneumonia  in  tabes,  164 
Poirier,  lymphatics  in  optic  nerve, 

13 
Posterior  column  fibers,  cerebellar, 

29 

medullary,  29 
spinal,  29 
Posterior     nerve     root,      central 

process,  course  of,  22 
situation  of,  18 
structure  of,  18 
Posterior  root  coverings,  18 
ganglion,  18 
ganglion  cells,  18,  19 
Posterior  root  lesion,   anatomical 

result  of,  39 
and  meningitis,  20 


Posterior  root  lesion,  and  spinal 

ganglion  cell,  19,  20 
effect  on  radiation  of,  39 
in  optic  atrophy,  frequency  of, 

12 

in  paresis,  frequency  of,  12 
physiological  result  of,  39 
primary,  21 

reflex  disintegration  of,  39 
results,  anatomical,  22 
results  of  complete,  51 
results  of  incomplete,  51,  52 
spread  of,  21 

Posterior  root  lymphatics,  13 
Posterior  root   section   in   gastric 

crises,  220-221 

Posterior  roots,  site  of  ergot  le- 
sions, 14 
Postural  aids,  65 
Postural  appreciation,  effect  of  le- 
sions on,  56 

Postural  deterioration,  65,  66 
Postural  exercises,  249 

dosage  of,  250 

Postural  images,  peripheral  after- 
images of  movement,  55,  79 
Postural  loss  and  ataxia,  70 
Postural  loss,  distribution  of,  58 

measurement  of,  56 
Postural  sense,  normal  blind,  59 

tabetic  blind,  59 
Postural  suppression  and  fear,  68 

and  visual  substitution,  67 
Postural  threshold,  normal  varia- 
tions of,  57 
Posture  and  fear,  68 
Posture,  factors  in,  62 
influence  of  mental  state,  62 
its  acquirement,  61 
its  maintenance,  62 
sensation  of,  55 
Pre-ataxic  period,  159 

duration  of,  Fournier,  159 
Grossman,  160 


INDEX 


295 


Pre-ataxic  stage,  duration  of,  77 

Predilection,  cultural,  16 

Pressure  pain  loss,  124-125 
distribution  of,  125 

Pressure  pain,  relation  to  the  veg- 
etative nervous  system,  120- 
124 

Pressure  sense,  relation  to  vege- 
tative nervous  system,  120- 
124 

Pretabetic    period,     duration    of, 

Grossman,  157 
Lowinsky,  157 

Pretabetic  period,  effect  of  drugs 
on  duration  of,  167 

Prevention  of  Rombergism,  205 

Principles  of  psychological  treat- 
ment, 188 

Principles  of  treating  mental 
state,  188 

Progression,  training  in,  256 

Properties  of  reflex  action,  27 

Protected  tissues,  syphilitic  inva- 
sion, 11 

Psychological  treatment,  princi- 
ples of,  188 

Psychoses  of  tabes,  178 

Psychotherapy,  principles  of,  188 

Pupil,  Argyll-Robertson,  119 
changes  in  tabes,  118,  119 
mechanism  of  movement,  118 

Racial  incidence  of  tabes,  147 

Radiation,  27 

Reciprocal     relations     of    mental 

state  and  symptoms,  185 
Reckoning  test  in  tabes,  177-182 

mode  of  use,  180-181 
Recumbent  posture,  249 
Reflex  action,  agonists  and  antag- 
onists, 28 

properties,  27 

reflex  arc,  afferent  path,  24 

synergic,  28 


Reflex  collateral,  course,  22 
Reflex    defect    during    voluntary 

movement,  44 
Reflex  disintegration,  difficulty  of 

measurement,  42 
initial  and  ultimate  results,  39 
rapidity  of  development  of  le- 
sions, 39 
site  of  lesion,  40 
Reflex  loss  and  ataxia,  70 
Reflex  theory  of  ataxia,  69 
Reflexes,  deep,  32,  33 

tendon,  32,  33 

Reinforcement   of  reflex  by   cor- 
tical action,  43 

Relation    of    antisyphilitic    treat- 
ment to  tabes,  168 
Relation  of  meningitis  to  posterior 

root  lesion,  20 

Relation  of  spinal  ganglion  cell  to 
posterior  root  lesion,  19,  20 
Relay,  law  of,  39 
Remissions  in  tabes,  159 
Renal  diseases  in  tabes,  164 
Resistance  exercises,  251 
Resistance  in   degenerated   nerve, 

52 

Resistance   of  nerve  cells,  varia- 
tions in,  14 

Resistance  in  synapse  of  degen- 
erated nerve,  52 
Resistance,  synapse,  seat  of,  27 
Rest  exercises,  196-204 
Rest    exercises,    effect,    on    blood 

pressure,   200-201 
on  pulse,  201 
on  musculature,  200 
on  mental  state,  200,  202 
Rest    exercises,    physiological    ef- 
fects of,  200 

routine  procedure  in,  202 
Romberg,  recognition  of  tabes,  1 
Rombergism,  diagnosis  of,  64 
mechanism  of,  57,  58 


296 


INDEX 


Rombergism,  measurement  of,  65, 
226 

prevention  of,  205-227 
Romberg's  sign,  63 

analysis,  227 

eliciting  of,  63,  64 

first  motor  disability,  226 
Root  lesions  and  aortic  disease,  11 
Root  lesions.     See  posterior   and 

anterior  root  lesions 
Rydlewski,  psychoses  of  tabes,  178 

Salvarsan,  failure  in  treatment  of 

optic  atrophy,  169 
followed  by  fulminating  spread 

of  lesions,  146 

intraspinal  administration,  173 
Salvarsanised  serum,  173 
Secondary  lesions,  specific  spiro- 

chete,  5 

Senile  tabes,  146 

Sensation,     complexity     of     sim- 
plest, 50 

Sense  of  pressure,  relation  to  the 
vegetative  nervous   system, 
120-124 
Sensory  images,  fate  of,  47,  48 

specificity  of,  47 
Sensory  impulses,  delayed  by  de- 
generation, 52 
speed  of,  52 
specific,  45 
Sensory  loss  and  ataxia,  70 

distribution  of,  52,  53 
Sensory  nerve  of  voluntary  mus- 
cle, origin,  course,  termina- 
tion of,  22 
Sensory  receptors,  24 
specificity  of,  45 
of  muscular  apparatus,  54,  55 
Sensory  theory  of  ataxia,  69 
Sensory  threshold,  estimation  of, 

48,  49 
variations  of,  48,  49 


Sequence  of  lesions,  16 
Seventh  nerve  lesions,  110,  122 
Sex  incidence  of  tabes,  147 
Shock  as  a  cause  of  tabes,  146 
Shoe,  tabetic,  238 
Signs,   influence   of  mental   state 

on,  185 

Sign  Romberg,  63 
Simple  reflex  arc,  mechanism  of, 

24 

Site    of    initial    attack,    determi- 
nants of,  15 

Sites  attacked  in  tabes,  12 
Sites  of  syphilis  in  central  nervous 

system,  12 
Sitting  posture,  249 
Slinger    and     Horsley,     postural 

sense  in  the  blind,  59 
Specific  strains  of  spirochetes,  5 
Spinal  integration,  28 
Spinal  tabes,  cause  of  progressive 

nature  of,  149 
Spinal  vegetative  fibers,  119 
Spirochete,  accessibility  of  tissues, 

5 

distribution,   13,   14 
exciting  organism  of  tabes,  5 
in  lymphatic  channels  of  nerves, 

13 

in  tabes,  Noguchi's  discovery,  4 
of  nervous  lesions,  5 
of  secondary  lesions,  5 
of  tertiary  lesions,  5 
persisting,  11 
specific  strains,  5 
Spread  of  invasion,  determinants 

of,  16 

Squint.     See  strabismus 
Stability,  mechanical  aids  to,  240- 

241 

Standing  posture,  249 
Stargardt  on  optic  tabes,  87 
Stargardt,    posterior    root    lesion 
parenchymatous,  21 


INDEX 


297 


Strabismus,  107-109 

cure  of,  207 
Strumpell,  aortic  disease  and  root 

lesions,  11 
Suppression    of   postural    images, 

57,  58 

of  visual  images,  107 
Swaying,   measurement    of,    ceph- 

alograph,  65 
normal,  62,  63 
Sympathetic  fibers,  117,  118 

lesions  in  tabes,  13 
Symptomatic    treatment,    psycho- 
therapeutic,  188 

Symptoms  and  signs  of  tabes,  151 
Symptoms,  effect  on  mental  state, 

184 
measurement    and    analysis    of, 

215 

of  fatigue,  176 
of  fear,  176-177 
pre-ataxic,  215 
prevention  of,  212-214 
Synapse,  cells,  changes  in  tabes, 

24 

Synergia,  center  of,  31 
Synergic  action,  28 
Syphilis  a  general  infection.  5 
causal  relation  to  tabes,  2 
in  central  nervous  system,  sites 

of,  12 

Syphilis   of  central   nervous   sys- 
tem,    constitutional     influ- 
ences of,  12 
liability  to,  12 

occupational  influences  of,  12 
spread  of,  abortive,  159 
fulminating,  156,  158 
tardy,  157,  158 

environmental  influences  affect- 
ing, 12 

Syphilis,  prosecution  for,  192-193 
Syphilitic    invasion    of    protected 
tissues,  11 


Syphilitic  neurasthenia,  153 
treatment  of,  190,  191,  192 

Tabes,  abducens  lesions,  13 
age  at  death,  163 
age  at  onset,  162,  163 
and  thyroid  gland,  146 
anterior  horn  cell  lesions,  13 
causes  of  death  in,  164 
cerebellar  lesions,  13 
cerebrospinal  fluid  in,  152 
cortical  lesions,  12,  13 
diagnosis  of,  153 
discovery  of,  1 
motor  nerve  lesions,  13 
occupational  incidence,  147 
occurrence  of  syphilis  in,  2 
oculomotor  lesions  in,  13 
producing  depression,  177 
producing  fatigue,  176 
pupillary  changes  in,  118,  119 
racial  incidence  of,  147 
senile,  146 

sex  incidence  of,  147 
sites  attacked,  12 
sympathetic  lesions  of,  13 
symptoms  and  signs  of,  151 
theories  of  causation  of,  2 
types  of,  162 
vagus  lesions,  13 
vestibular  lesions,  13 
Wassermann  reaction  in,  152 

Tabetic  boot,  238 
deafness,  course  of,  114-115 
incipient,  treatment  of,  190-192 

Tabetic  lesions,  affecting  micturi- 
tion,  132 
and  ataxia,  73,  74 
anterior  horn  cell,  frequency,  re- 
sult of,  37 
auditory,  13 
cerebellar,  13 

cochlear  nerve,  extent  of,  114 
result  of,  114 


298 


INDEX 


Tabetic   lesions,   compatible   with 
syphilitic  origin,  4 

cortical,  12,  13 

cranial  nerves,  86 

eighth    nerve.      See    vestibular 
and  cochlear 

fifth  nerve,  110 

inflammatory,  not  toxic,  4 

motor  nerve,  13 

motor  nerve,  results  of,  37 

oculomotor,  13 

olfactory,  87 

optic,  12,  87 

peripheral  nerves,  12,  13 

peripheral   processes   of  spinal 
ganglion  cell,  19 

posterior  root,  meninges,  19 

seventh,  110 

spinal  ganglion  cells,  18,  19 

sympathetic,  13 

vagal,  13 

vestibular,  13 
Tabetic,    potential    treatment    of, 

190-192 
Tabetic,   pre-ataxic  treatment  of, 

194 
Tabetic  psychosis,  178 

shoe,  238 

signs,  anatomical  basis  of,  152 

symptoms,  interdependence,  186 
Tactile  sensibility  loss,  53 
Temperature,  loss,  53 
Tendon  reflexes,  32,  33 
Theories  of  ataxia,  69 
Theory,  drainage,  28 

James,  195 
Threshold  of  ataxia,  78 

of  change  of  illumination,  90 

of  direction  of  movement,  58 

of  light  perception,  90 

of  movement,  57 
Thyroid  gland  in  tabes,  146 
Tissue    immunity    to    spirochetes, 
138,  139 


Toe  clutching,  230 
Toes,  callous  formation  on,  231 
Training  in  cerebral  control,  204, 
205,  206 

in  direction,  251,  252 

in  extent,  251,  252 

in  mental  capacity,  207 

in  rhythm,  251 
Treatment  by  drugs,  166 

curative,  166 

preventive,  166 
Treatment  of  arthropathies,  261 

of  blindness,  223 

of  deafness,  224 

of  incipient  tabes,  190-192 

of  involuntary  micturition,  222- 
223 

of  optic  atrophy,  223 

of  syphilitic  neurasthenia,  190- 

192 

Trigeminal  lesions.    See  fifth 
Trunk  exercises,  253 
Tuberculosis  in  tabes,  164 
Types    of   persisting   spirochetes, 
11 

Urination.     See  micturition 

Vagal  fibers,  117,  118 

irritation  and  gastric  crises,  128 
Vagotonia,  precursor  of  tabes,  153 

treatment  of,  190-191 
Vagus  lesions  in  tabes,  13 
Vascular  disease  in  tabes,  164 
Vegetative  nervous  system,  affer- 
ent and  efferent  spinal  fi- 
bers, 119 
chemical  stimulation  to  defense, 

145 

composition  of,  117 
development  of,  117 
Vegetative  nervous  system  lesions, 

arthropathies,  137,  138 
atrophies,  137 


INDEX 


299 


Vegetative  nervous  system  lesions, 

effect  on  defense,  150 
fractures,  137 
infections,  137 
trophic  ulcers,  137 
Vegetative  nervous  system,  mental 

control  of,  150 
plexuses,  119 

relation  of  spinal  afferent  to 
posterior  root  ganglion, 
120-124 

sensory  function  of,  120-124 
Vegetative  nervous  system,  spino- 

medullary  centers,  119 
and  metabolism,  136 
Vestibular  impulses,  origin,  distri- 
bution of,  29 
lesions  in  tabes,  13 


Vestibular    lesions,    detection    of, 

111 

Vestibular  organ   of  tone,   situa- 
tion, receptors  of,  29,  30 
Vibration,  loss  of,  54 
Virility  and  mental  state,  130 
Visual  criticism  of  movement,  80 
Visual  images,  detection  of  sup- 
pression of,  107 

Visually  directed  movements,  245 
Von  Frey's  hairs,  47,  48 

Walking  in  tabes,  258,  260 
Wassermann  reaction  in  tabes,  152 
Wilson,    anterior    horn    cells    in 

tabes,  13 

Wittmarck's  experiments,  111-112 
Wolf,  cure  of  ataxia,  274 
(i) 


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SEP  2  2  1992 

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3  RECB 

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HP 

1986 

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